[{"publisher":"Cold Spring Harbor Laboratory","main_file_link":[{"url":"https://doi.org/10.1101/2023.11.30.569337","open_access":"1"}],"oa":1,"month":"12","abstract":[{"lang":"eng","text":"In the developing vertebrate central nervous system, neurons and glia typically arise sequentially from common progenitors. Here, we report that the transcription factor Forkhead Box G1 (Foxg1) regulates gliogenesis in the mouse neocortex via distinct cell-autonomous roles in progenitors and in postmitotic neurons that regulate different aspects of the gliogenic FGF signalling pathway. We demonstrate that loss of Foxg1 in cortical progenitors at neurogenic stages causes premature astrogliogenesis. We identify a novel FOXG1 target, the pro-gliogenic FGF pathway component Fgfr3, which is suppressed by FOXG1 cell-autonomously to maintain neurogenesis. Furthermore, FOXG1 can also suppress premature astrogliogenesis triggered by the augmentation of FGF signalling. We identify a second novel function of FOXG1 in regulating the expression of gliogenic ligand FGF18 in new born neocortical upper-layer neurons. Loss of FOXG1 in postmitotic neurons increases Fgf18 expression and enhances gliogenesis in the progenitors. These results fit well with the model that new born neurons secrete cues that trigger progenitors to produce the next wave of cell types, astrocytes. If FGF signalling is attenuated in Foxg1 null progenitors, they progress to oligodendrocyte production. Therefore, loss of FOXG1 transitions the progenitor to a gliogenic state, producing either astrocytes or oligodendrocytes depending on FGF signalling levels. Our results uncover how FOXG1 integrates extrinsic signalling via the FGF pathway to regulate the sequential generation of neurons, astrocytes, and oligodendrocytes in the cerebral cortex."}],"oa_version":"Preprint","acknowledgement":"We thank Dr. Shital Suryavanshi and the animal house staff of the Tata Institute of\r\nFundamental Research (TIFR) for their excellent support; Gord Fishell and Goichi Miyoshi for\r\nthe Foxg1 floxed mouse line; Hiroshi Kawasaki for the plasmids pCAG-FGF8 and pCAGsFGFR3c. We thank Prof. S.K. Lee for the Foxg1lox/lox genotyping primers and protocol. We thank Dr. Deepak Modi and Dr. Vainav Patel for allowing us to use the NIRRCH FACS Facility and the staff of the NIRRCH and TIFR FACS facilities for their assistance.\r\nWe thank Denis Jabaudon for his critical comments on the manuscript and members of the\r\nJabaudon lab for helpful discussions. This work was funded by the Department of Atomic\r\nEnergy (DAE), Govt. of India (Project Identification no. RTI4003, DAE OM no.\r\n1303/2/2019/R&D-II/DAE/2079).","date_published":"2023-12-01T00:00:00Z","doi":"10.1101/2023.11.30.569337","date_created":"2023-12-06T13:07:01Z","year":"2023","publication_status":"submitted","day":"01","publication":"bioRxiv","language":[{"iso":"eng"}],"type":"preprint","status":"public","_id":"14647","author":[{"first_name":"Mahima","last_name":"Bose","full_name":"Bose, Mahima"},{"first_name":"Varun","last_name":"Suresh","full_name":"Suresh, Varun"},{"full_name":"Mishra, Urvi","last_name":"Mishra","first_name":"Urvi"},{"first_name":"Ishita","last_name":"Talwar","full_name":"Talwar, Ishita"},{"first_name":"Anuradha","last_name":"Yadav","full_name":"Yadav, Anuradha"},{"full_name":"Biswas, Shiona","last_name":"Biswas","first_name":"Shiona"},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"},{"full_name":"Tole, Shubha","last_name":"Tole","first_name":"Shubha"}],"article_processing_charge":"No","department":[{"_id":"SiHi"}],"title":"Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway","citation":{"chicago":"Bose, Mahima, Varun Suresh, Urvi Mishra, Ishita Talwar, Anuradha Yadav, Shiona Biswas, Simon Hippenmeyer, and Shubha Tole. “Dual Role of FOXG1 in Regulating Gliogenesis in the Developing Neocortex via the FGF Signalling Pathway.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2023.11.30.569337.","ista":"Bose M, Suresh V, Mishra U, Talwar I, Yadav A, Biswas S, Hippenmeyer S, Tole S. Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway. bioRxiv, 10.1101/2023.11.30.569337.","mla":"Bose, Mahima, et al. “Dual Role of FOXG1 in Regulating Gliogenesis in the Developing Neocortex via the FGF Signalling Pathway.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2023.11.30.569337.","apa":"Bose, M., Suresh, V., Mishra, U., Talwar, I., Yadav, A., Biswas, S., … Tole, S. (n.d.). Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2023.11.30.569337","ama":"Bose M, Suresh V, Mishra U, et al. Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway. bioRxiv. doi:10.1101/2023.11.30.569337","ieee":"M. Bose et al., “Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway,” bioRxiv. Cold Spring Harbor Laboratory.","short":"M. Bose, V. Suresh, U. Mishra, I. Talwar, A. Yadav, S. Biswas, S. Hippenmeyer, S. Tole, BioRxiv (n.d.)."},"date_updated":"2023-12-11T07:37:17Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87"},{"publication_status":"epub_ahead","publication_identifier":{"issn":["2666-1667"]},"language":[{"iso":"eng"}],"ec_funded":1,"volume":5,"issue":"1","abstract":[{"lang":"eng","text":"Mosaic analysis with double markers (MADM) technology enables the generation of genetic mosaic tissue in mice and high-resolution phenotyping at the individual cell level. Here, we present a protocol for isolating MADM-labeled cells with high yield for downstream molecular analyses using fluorescence-activated cell sorting (FACS). We describe steps for generating MADM-labeled mice, perfusion, single-cell suspension, and debris removal. We then detail procedures for cell sorting by FACS and downstream analysis. This protocol is suitable for embryonic to adult mice.\r\nFor complete details on the use and execution of this protocol, please refer to Contreras et al. (2021).1"}],"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"pmid":1,"oa_version":"Submitted Version","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.xpro.2023.102771"}],"scopus_import":"1","intvolume":" 5","month":"12","date_updated":"2023-12-18T08:06:14Z","ddc":["570"],"department":[{"_id":"SiHi"}],"_id":"14683","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"review","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Neuroscience"],"status":"public","year":"2023","publication":"STAR Protocols","day":"08","date_created":"2023-12-13T11:48:05Z","date_published":"2023-12-08T00:00:00Z","doi":"10.1016/j.xpro.2023.102771","acknowledgement":"This research was supported by the Scientific Service Units (SSU) at IST Austria through resources provided by the Imaging & Optics Facility (IOF) and Preclinical Facilities (PCF). N.A. received support from FWF Firnberg-Programme (T 1031). G.C. received support from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 754411 as an ISTplus postdoctoral fellow. This work was also supported by IST Austria institutional funds, FWF SFB F78 to S.H., and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 725780 LinPro) to S.H.","oa":1,"publisher":"Elsevier","quality_controlled":"1","citation":{"mla":"Amberg, Nicole, et al. “Protocol for Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers by Flow Cytometry.” STAR Protocols, vol. 5, no. 1, 102771, Elsevier, 2023, doi:10.1016/j.xpro.2023.102771.","ama":"Amberg N, Cheung GT, Hippenmeyer S. Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols. 2023;5(1). doi:10.1016/j.xpro.2023.102771","apa":"Amberg, N., Cheung, G. T., & Hippenmeyer, S. (2023). Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2023.102771","ieee":"N. Amberg, G. T. Cheung, and S. Hippenmeyer, “Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry,” STAR Protocols, vol. 5, no. 1. Elsevier, 2023.","short":"N. Amberg, G.T. Cheung, S. Hippenmeyer, STAR Protocols 5 (2023).","chicago":"Amberg, Nicole, Giselle T Cheung, and Simon Hippenmeyer. “Protocol for Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers by Flow Cytometry.” STAR Protocols. Elsevier, 2023. https://doi.org/10.1016/j.xpro.2023.102771.","ista":"Amberg N, Cheung GT, Hippenmeyer S. 2023. Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols. 5(1), 102771."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","external_id":{"pmid":["38070137"]},"author":[{"last_name":"Amberg","orcid":"0000-0002-3183-8207","full_name":"Amberg, Nicole","first_name":"Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Cheung","full_name":"Cheung, Giselle T","orcid":"0000-0001-8457-2572","first_name":"Giselle T","id":"471195F6-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"title":"Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry","article_number":"102771","project":[{"call_identifier":"FWF","_id":"268F8446-B435-11E9-9278-68D0E5697425","name":"Role of Eed in neural stem cell lineage progression","grant_number":"T0101031"},{"_id":"260C2330-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"ISTplus - Postdoctoral Fellowships","grant_number":"754411"},{"_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E","name":"Molecular Mechanisms of Neural Stem Cell Lineage Progression","grant_number":"F07805"},{"call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780"}]},{"oa_version":"None","abstract":[{"text":"The cerebral cortex is comprised of a vast cell-type diversity sequentially generated by cortical progenitor cells. Faithful progenitor lineage progression requires the tight orchestration of distinct molecular and cellular mechanisms regulating proper progenitor proliferation behavior and differentiation. Correct execution of developmental programs involves a complex interplay of cell intrinsic and tissue-wide mechanisms. Many studies over the past decades have been able to determine a plethora of genes critically involved in cortical development. However, only a few made use of genetic paradigms with sparse and global gene deletion to probe cell-autonomous vs. tissue-wide contribution. In this chapter, we will elaborate on the importance of dissecting the cell-autonomous and tissue-wide mechanisms to gain a precise understanding of gene function during radial glial progenitor lineage progression.","lang":"eng"}],"month":"08","publisher":"Wiley","scopus_import":"1","quality_controlled":"1","day":"08","language":[{"iso":"eng"}],"publication":"Neocortical Neurogenesis in Development and Evolution","publication_identifier":{"eisbn":["9781119860914"]},"publication_status":"published","year":"2023","doi":"10.1002/9781119860914.ch10","date_published":"2023-08-08T00:00:00Z","date_created":"2024-01-08T13:16:36Z","page":"169-191","_id":"14757","status":"public","type":"book_chapter","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2024-01-09T09:46:57Z","citation":{"apa":"Villalba Requena, A., Amberg, N., & Hippenmeyer, S. (2023). Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression. In W. Huttner (Ed.), Neocortical Neurogenesis in Development and Evolution (pp. 169–191). Wiley. https://doi.org/10.1002/9781119860914.ch10","ama":"Villalba Requena A, Amberg N, Hippenmeyer S. Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression. In: Huttner W, ed. Neocortical Neurogenesis in Development and Evolution. Wiley; 2023:169-191. doi:10.1002/9781119860914.ch10","ieee":"A. Villalba Requena, N. Amberg, and S. Hippenmeyer, “Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression,” in Neocortical Neurogenesis in Development and Evolution, W. Huttner, Ed. Wiley, 2023, pp. 169–191.","short":"A. Villalba Requena, N. Amberg, S. Hippenmeyer, in:, W. Huttner (Ed.), Neocortical Neurogenesis in Development and Evolution, Wiley, 2023, pp. 169–191.","mla":"Villalba Requena, Ana, et al. “Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression.” Neocortical Neurogenesis in Development and Evolution, edited by Wieland Huttner, Wiley, 2023, pp. 169–91, doi:10.1002/9781119860914.ch10.","ista":"Villalba Requena A, Amberg N, Hippenmeyer S. 2023.Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression. In: Neocortical Neurogenesis in Development and Evolution. , 169–191.","chicago":"Villalba Requena, Ana, Nicole Amberg, and Simon Hippenmeyer. “Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression.” In Neocortical Neurogenesis in Development and Evolution, edited by Wieland Huttner, 169–91. Wiley, 2023. https://doi.org/10.1002/9781119860914.ch10."},"department":[{"_id":"SiHi"}],"editor":[{"full_name":"Huttner, Wieland","last_name":"Huttner","first_name":"Wieland"}],"title":"Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression","author":[{"full_name":"Villalba Requena, Ana","orcid":"0000-0002-5615-5277","last_name":"Villalba Requena","id":"68cb85a0-39f7-11eb-9559-9aaab4f6a247","first_name":"Ana"},{"full_name":"Amberg, Nicole","orcid":"0000-0002-3183-8207","last_name":"Amberg","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","first_name":"Nicole"},{"orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"}],"article_processing_charge":"No"},{"month":"04","intvolume":" 12","abstract":[{"text":"Connexin 43, an astroglial gap junction protein, is enriched in perisynaptic astroglial processes and plays major roles in synaptic transmission. We have previously found that astroglial Cx43 controls synaptic glutamate levels and allows for activity-dependent glutamine release to sustain physiological synaptic transmissions and cognitiogns. However, whether Cx43 is important for the release of synaptic vesicles, which is a critical component of synaptic efficacy, remains unanswered. Here, using transgenic mice with a glial conditional knockout of Cx43 (Cx43−/−), we investigate whether and how astrocytes regulate the release of synaptic vesicles from hippocampal synapses. We report that CA1 pyramidal neurons and their synapses develop normally in the absence of astroglial Cx43. However, a significant impairment in synaptic vesicle distribution and release dynamics were observed. In particular, the FM1-43 assays performed using two-photon live imaging and combined with multi-electrode array stimulation in acute hippocampal slices, revealed a slower rate of synaptic vesicle release in Cx43−/− mice. Furthermore, paired-pulse recordings showed that synaptic vesicle release probability was also reduced and is dependent on glutamine supply via Cx43 hemichannel (HC). Taken together, we have uncovered a role for Cx43 in regulating presynaptic functions by controlling the rate and probability of synaptic vesicle release. Our findings further highlight the significance of astroglial Cx43 in synaptic transmission and efficacy.","lang":"eng"}],"pmid":1,"oa_version":"Published Version","issue":"8","volume":12,"publication_identifier":{"issn":["2073-4409"]},"publication_status":"published","file":[{"checksum":"6798cd75d8857976fbc58a43fd173d68","file_id":"14808","success":1,"content_type":"application/pdf","access_level":"open_access","relation":"main_file","date_created":"2024-01-16T09:26:52Z","file_name":"2023_Cells_Cheung.pdf","date_updated":"2024-01-16T09:26:52Z","file_size":7931643,"creator":"dernst"}],"language":[{"iso":"eng"}],"article_type":"original","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","keyword":["General Medicine"],"_id":"14783","file_date_updated":"2024-01-16T09:26:52Z","department":[{"_id":"SiHi"}],"date_updated":"2024-01-16T09:29:35Z","ddc":["570"],"publisher":"MDPI","quality_controlled":"1","oa":1,"acknowledgement":"This research was funded by grants from the European Research Council (Consolidator grant #683154) and European Union’s Horizon 2020 research and innovation program (Marie Sklodowska-Curie Innovative Training Networks, grant #722053, EU-GliaPhD) to N.R., as well as from FP7-PEOPLE Marie Curie Intra-European Fellowship for career development (grant #622289) to G.C. We thank Elena Dossi, Grégory Ghézali, and Jérémie Teillon for support with setting up the MEA system for the two-photon microscope. We would also like to thank Tayfun Palaz for their technical assistance with the EM preparations.","date_published":"2023-04-11T00:00:00Z","doi":"10.3390/cells12081133","date_created":"2024-01-10T09:46:35Z","isi":1,"has_accepted_license":"1","year":"2023","day":"11","publication":"Cells","article_number":"1133","author":[{"id":"471195F6-F248-11E8-B48F-1D18A9856A87","first_name":"Giselle T","last_name":"Cheung","orcid":"0000-0001-8457-2572","full_name":"Cheung, Giselle T"},{"full_name":"Chever, Oana","last_name":"Chever","first_name":"Oana"},{"last_name":"Rollenhagen","full_name":"Rollenhagen, Astrid","first_name":"Astrid"},{"first_name":"Nicole","last_name":"Quenech’du","full_name":"Quenech’du, Nicole"},{"last_name":"Ezan","full_name":"Ezan, Pascal","first_name":"Pascal"},{"last_name":"Lübke","full_name":"Lübke, Joachim H. R.","first_name":"Joachim H. R."},{"first_name":"Nathalie","full_name":"Rouach, Nathalie","last_name":"Rouach"}],"article_processing_charge":"Yes","external_id":{"isi":["000977445700001"],"pmid":["37190042"]},"title":"Astroglial connexin 43 regulates synaptic vesicle release at hippocampal synapses","citation":{"ama":"Cheung GT, Chever O, Rollenhagen A, et al. Astroglial connexin 43 regulates synaptic vesicle release at hippocampal synapses. Cells. 2023;12(8). doi:10.3390/cells12081133","apa":"Cheung, G. T., Chever, O., Rollenhagen, A., Quenech’du, N., Ezan, P., Lübke, J. H. R., & Rouach, N. (2023). Astroglial connexin 43 regulates synaptic vesicle release at hippocampal synapses. Cells. MDPI. https://doi.org/10.3390/cells12081133","short":"G.T. Cheung, O. Chever, A. Rollenhagen, N. Quenech’du, P. Ezan, J.H.R. Lübke, N. Rouach, Cells 12 (2023).","ieee":"G. T. Cheung et al., “Astroglial connexin 43 regulates synaptic vesicle release at hippocampal synapses,” Cells, vol. 12, no. 8. MDPI, 2023.","mla":"Cheung, Giselle T., et al. “Astroglial Connexin 43 Regulates Synaptic Vesicle Release at Hippocampal Synapses.” Cells, vol. 12, no. 8, 1133, MDPI, 2023, doi:10.3390/cells12081133.","ista":"Cheung GT, Chever O, Rollenhagen A, Quenech’du N, Ezan P, Lübke JHR, Rouach N. 2023. Astroglial connexin 43 regulates synaptic vesicle release at hippocampal synapses. Cells. 12(8), 1133.","chicago":"Cheung, Giselle T, Oana Chever, Astrid Rollenhagen, Nicole Quenech’du, Pascal Ezan, Joachim H. R. Lübke, and Nathalie Rouach. “Astroglial Connexin 43 Regulates Synaptic Vesicle Release at Hippocampal Synapses.” Cells. MDPI, 2023. https://doi.org/10.3390/cells12081133."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87"},{"citation":{"short":"L. Knaus, B. Basilico, D. Malzl, M. Gerykova Bujalkova, M. Smogavec, L.A. Schwarz, S. Gorkiewicz, N. Amberg, F. Pauler, C. Knittl-Frank, M. Tassinari, N. Maulide, T. Rülicke, J. Menche, S. Hippenmeyer, G. Novarino, Cell 186 (2023) 1950–1967.e25.","ieee":"L. Knaus et al., “Large neutral amino acid levels tune perinatal neuronal excitability and survival,” Cell, vol. 186, no. 9. Elsevier, p. 1950–1967.e25, 2023.","apa":"Knaus, L., Basilico, B., Malzl, D., Gerykova Bujalkova, M., Smogavec, M., Schwarz, L. A., … Novarino, G. (2023). Large neutral amino acid levels tune perinatal neuronal excitability and survival. Cell. Elsevier. https://doi.org/10.1016/j.cell.2023.02.037","ama":"Knaus L, Basilico B, Malzl D, et al. Large neutral amino acid levels tune perinatal neuronal excitability and survival. Cell. 2023;186(9):1950-1967.e25. doi:10.1016/j.cell.2023.02.037","mla":"Knaus, Lisa, et al. “Large Neutral Amino Acid Levels Tune Perinatal Neuronal Excitability and Survival.” Cell, vol. 186, no. 9, Elsevier, 2023, p. 1950–1967.e25, doi:10.1016/j.cell.2023.02.037.","ista":"Knaus L, Basilico B, Malzl D, Gerykova Bujalkova M, Smogavec M, Schwarz LA, Gorkiewicz S, Amberg N, Pauler F, Knittl-Frank C, Tassinari M, Maulide N, Rülicke T, Menche J, Hippenmeyer S, Novarino G. 2023. Large neutral amino acid levels tune perinatal neuronal excitability and survival. Cell. 186(9), 1950–1967.e25.","chicago":"Knaus, Lisa, Bernadette Basilico, Daniel Malzl, Maria Gerykova Bujalkova, Mateja Smogavec, Lena A. Schwarz, Sarah Gorkiewicz, et al. “Large Neutral Amino Acid Levels Tune Perinatal Neuronal Excitability and Survival.” Cell. Elsevier, 2023. https://doi.org/10.1016/j.cell.2023.02.037."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","author":[{"first_name":"Lisa","id":"3B2ABCF4-F248-11E8-B48F-1D18A9856A87","full_name":"Knaus, Lisa","last_name":"Knaus"},{"full_name":"Basilico, Bernadette","orcid":"0000-0003-1843-3173","last_name":"Basilico","id":"36035796-5ACA-11E9-A75E-7AF2E5697425","first_name":"Bernadette"},{"full_name":"Malzl, Daniel","last_name":"Malzl","first_name":"Daniel"},{"full_name":"Gerykova Bujalkova, Maria","last_name":"Gerykova Bujalkova","first_name":"Maria"},{"full_name":"Smogavec, Mateja","last_name":"Smogavec","first_name":"Mateja"},{"full_name":"Schwarz, Lena A.","last_name":"Schwarz","first_name":"Lena A."},{"first_name":"Sarah","id":"f141a35d-15a9-11ec-9fb2-fef6becc7b6f","full_name":"Gorkiewicz, Sarah","last_name":"Gorkiewicz"},{"first_name":"Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","last_name":"Amberg","full_name":"Amberg, Nicole","orcid":"0000-0002-3183-8207"},{"id":"48EA0138-F248-11E8-B48F-1D18A9856A87","first_name":"Florian","last_name":"Pauler","orcid":"0000-0002-7462-0048","full_name":"Pauler, Florian"},{"first_name":"Christian","full_name":"Knittl-Frank, Christian","last_name":"Knittl-Frank"},{"first_name":"Marianna","id":"7af593f1-d44a-11ed-bf94-a3646a6bb35e","full_name":"Tassinari, Marianna","last_name":"Tassinari"},{"first_name":"Nuno","last_name":"Maulide","full_name":"Maulide, Nuno"},{"first_name":"Thomas","full_name":"Rülicke, Thomas","last_name":"Rülicke"},{"full_name":"Menche, Jörg","last_name":"Menche","first_name":"Jörg"},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"},{"first_name":"Gaia","id":"3E57A680-F248-11E8-B48F-1D18A9856A87","last_name":"Novarino","full_name":"Novarino, Gaia","orcid":"0000-0002-7673-7178"}],"external_id":{"isi":["000991468700001"]},"article_processing_charge":"Yes (via OA deal)","title":"Large neutral amino acid levels tune perinatal neuronal excitability and survival","project":[{"name":"Molecular Drug Targets","grant_number":"W1232-B24","call_identifier":"FWF","_id":"2548AE96-B435-11E9-9278-68D0E5697425"},{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"grant_number":"715508","name":"Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo and in vitro Models","_id":"25444568-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}],"isi":1,"has_accepted_license":"1","year":"2023","day":"27","publication":"Cell","page":"1950-1967.e25","date_published":"2023-04-27T00:00:00Z","doi":"10.1016/j.cell.2023.02.037","date_created":"2023-04-05T08:15:40Z","acknowledgement":"We thank A. Freeman and V. Voronin for technical assistance, S. Deixler, A. Stichelberger, M. Schunn, and the Preclinical Facility for managing our animal colony. We thank L. Andersen and J. Sonntag, who were involved in generating the MADM lines. We thank the ISTA LSF Mass Spectrometry Core Facility for assistance with the proteomic analysis, as well as the ISTA electron microscopy and Imaging and Optics facility for technical support. Metabolomics LC-MS/MS analysis was performed by the Metabolomics Facility at Vienna BioCenter Core Facilities (VBCF). We acknowledge the support of the EMBL Metabolomics Core Facility (MCF) for lipidomics and intracellular metabolomics mass spectrometry data acquisition and analysis. RNA sequencing was performed by the Next Generation Sequencing Facility at VBCF. Schematics were generated using Biorender.com. This work was supported by the Austrian Science Fund (FWF, DK W1232-B24) and by the European Union’s Horizon 2020 research and innovation program (ERC) grant 725780 (LinPro) to S.H. and 715508 (REVERSEAUTISM) to G.N.","quality_controlled":"1","publisher":"Elsevier","oa":1,"date_updated":"2024-02-07T08:03:32Z","ddc":["570"],"file_date_updated":"2023-05-02T09:26:21Z","department":[{"_id":"SiHi"},{"_id":"GaNo"}],"_id":"12802","type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","keyword":["General Biochemistry","Genetics and Molecular Biology"],"publication_identifier":{"issn":["0092-8674"]},"publication_status":"published","file":[{"creator":"dernst","date_updated":"2023-05-02T09:26:21Z","file_size":15712841,"date_created":"2023-05-02T09:26:21Z","file_name":"2023_Cell_Knaus.pdf","access_level":"open_access","relation":"main_file","content_type":"application/pdf","checksum":"47e94fbe19e86505b429cb7a5b503ce6","file_id":"12889","success":1}],"language":[{"iso":"eng"}],"volume":186,"issue":"9","related_material":{"link":[{"url":"https://ista.ac.at/en/news/feed-them-or-lose-them/","relation":"press_release","description":"News on ISTA Website"}],"record":[{"relation":"dissertation_contains","status":"public","id":"13107"}]},"ec_funded":1,"abstract":[{"lang":"eng","text":"Little is known about the critical metabolic changes that neural cells have to undergo during development and how temporary shifts in this program can influence brain circuitries and behavior. Inspired by the discovery that mutations in SLC7A5, a transporter of metabolically essential large neutral amino acids (LNAAs), lead to autism, we employed metabolomic profiling to study the metabolic states of the cerebral cortex across different developmental stages. We found that the forebrain undergoes significant metabolic remodeling throughout development, with certain groups of metabolites showing stage-specific changes, but what are the consequences of perturbing this metabolic program? By manipulating Slc7a5 expression in neural cells, we found that the metabolism of LNAAs and lipids are interconnected in the cortex. Deletion of Slc7a5 in neurons affects the postnatal metabolic state, leading to a shift in lipid metabolism. Additionally, it causes stage- and cell-type-specific alterations in neuronal activity patterns, resulting in a long-term circuit dysfunction."}],"acknowledged_ssus":[{"_id":"PreCl"},{"_id":"EM-Fac"},{"_id":"Bio"},{"_id":"LifeSc"}],"oa_version":"Published Version","scopus_import":"1","month":"04","intvolume":" 186"},{"ddc":["570"],"date_updated":"2023-05-31T12:24:10Z","file_date_updated":"2023-03-21T14:18:10Z","department":[{"_id":"SiHi"}],"_id":"11336","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"original","type":"journal_article","language":[{"iso":"eng"}],"file":[{"content_type":"application/pdf","relation":"main_file","access_level":"open_access","success":1,"checksum":"0117023e188542082ca6693cf39e7f03","file_id":"12742","file_size":2973998,"date_updated":"2023-03-21T14:18:10Z","creator":"patrickd","file_name":"sciadv.abq1263.pdf","date_created":"2023-03-21T14:18:10Z"}],"publication_status":"published","publication_identifier":{"issn":["2375-2548"]},"ec_funded":1,"related_material":{"link":[{"relation":"press_release","url":"https://ista.ac.at/en/news/whole-tissue-shapes-brain-development/","description":"News on ISTA website"}]},"issue":"44","volume":8,"oa_version":"Published Version","abstract":[{"text":"The generation of a correctly-sized cerebral cortex with all-embracing neuronal and glial cell-type diversity critically depends on faithful radial glial progenitor (RGP) cell proliferation/differentiation programs. Temporal RGP lineage progression is regulated by Polycomb Repressive Complex 2 (PRC2) and loss of PRC2 activity results in severe neurogenesis defects and microcephaly. How PRC2-dependent gene expression instructs RGP lineage progression is unknown. Here we utilize Mosaic Analysis with Double Markers (MADM)-based single cell technology and demonstrate that PRC2 is not cell-autonomously required in neurogenic RGPs but rather acts at the global tissue-wide level. Conversely, cortical astrocyte production and maturation is cell-autonomously controlled by PRC2-dependent transcriptional regulation. We thus reveal highly distinct and sequential PRC2 functions in RGP lineage progression that are dependent on complex interplays between intrinsic and tissue-wide properties. In a broader context our results imply a critical role for the genetic and cellular niche environment in neural stem cell behavior.","lang":"eng"}],"acknowledged_ssus":[{"_id":"PreCl"},{"_id":"Bio"},{"_id":"LifeSc"}],"intvolume":" 8","month":"11","scopus_import":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"ama":"Amberg N, Pauler F, Streicher C, Hippenmeyer S. Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression. Science Advances. 2022;8(44). doi:10.1126/sciadv.abq1263","apa":"Amberg, N., Pauler, F., Streicher, C., & Hippenmeyer, S. (2022). Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression. Science Advances. American Association for the Advancement of Science. https://doi.org/10.1126/sciadv.abq1263","short":"N. Amberg, F. Pauler, C. Streicher, S. Hippenmeyer, Science Advances 8 (2022).","ieee":"N. Amberg, F. Pauler, C. Streicher, and S. Hippenmeyer, “Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression,” Science Advances, vol. 8, no. 44. American Association for the Advancement of Science, 2022.","mla":"Amberg, Nicole, et al. “Tissue-Wide Genetic and Cellular Landscape Shapes the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression.” Science Advances, vol. 8, no. 44, abq1263, American Association for the Advancement of Science, 2022, doi:10.1126/sciadv.abq1263.","ista":"Amberg N, Pauler F, Streicher C, Hippenmeyer S. 2022. Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression. Science Advances. 8(44), abq1263.","chicago":"Amberg, Nicole, Florian Pauler, Carmen Streicher, and Simon Hippenmeyer. “Tissue-Wide Genetic and Cellular Landscape Shapes the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression.” Science Advances. American Association for the Advancement of Science, 2022. https://doi.org/10.1126/sciadv.abq1263."},"title":"Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression","article_processing_charge":"No","author":[{"last_name":"Amberg","orcid":"0000-0002-3183-8207","full_name":"Amberg, Nicole","first_name":"Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Pauler, Florian","last_name":"Pauler","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","first_name":"Florian"},{"first_name":"Carmen","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","full_name":"Streicher, Carmen","last_name":"Streicher"},{"last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"article_number":"abq1263","project":[{"_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"},{"call_identifier":"FWF","_id":"268F8446-B435-11E9-9278-68D0E5697425","name":"Role of Eed in neural stem cell lineage progression","grant_number":"T0101031"}],"publication":"Science Advances","day":"01","year":"2022","has_accepted_license":"1","date_created":"2022-04-26T15:04:50Z","doi":"10.1126/sciadv.abq1263","date_published":"2022-11-01T00:00:00Z","acknowledgement":"We thank A. Heger (IST Austria Preclinical Facility), A. Sommer and C. Czepe (VBCF GmbH, NGS Unit) and S. Gharagozlou for technical support. This research was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Imaging & Optics Facility (IOF), Lab Support Facility (LSF), and Preclinical Facility (PCF). N.A. received funding from the FWF Firnberg-Programm (T 1031). The work was supported by IST institutional funds and by the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program (grant agreement 725780 LinPro) to S.H.","oa":1,"quality_controlled":"1","publisher":"American Association for the Advancement of Science"},{"month":"07","intvolume":" 23","scopus_import":"1","oa_version":"Published Version","acknowledged_ssus":[{"_id":"Bio"},{"_id":"EM-Fac"},{"_id":"PreCl"},{"_id":"LifeSc"}],"abstract":[{"lang":"eng","text":"Lymph nodes (LNs) comprise two main structural elements: fibroblastic reticular cells that form dedicated niches for immune cell interaction and capsular fibroblasts that build a shell around the organ. Immunological challenge causes LNs to increase more than tenfold in size within a few days. Here, we characterized the biomechanics of LN swelling on the cellular and organ scale. We identified lymphocyte trapping by influx and proliferation as drivers of an outward pressure force, causing fibroblastic reticular cells of the T-zone (TRCs) and their associated conduits to stretch. After an initial phase of relaxation, TRCs sensed the resulting strain through cell matrix adhesions, which coordinated local growth and remodeling of the stromal network. While the expanded TRC network readopted its typical configuration, a massive fibrotic reaction of the organ capsule set in and countered further organ expansion. Thus, different fibroblast populations mechanically control LN swelling in a multitier fashion."}],"volume":23,"ec_funded":1,"file":[{"success":1,"file_id":"11642","checksum":"628e7b49809f22c75b428842efe70c68","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_name":"2022_NatureImmunology_Assen.pdf","date_created":"2022-07-25T07:11:32Z","file_size":11475325,"date_updated":"2022-07-25T07:11:32Z","creator":"dernst"}],"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["1529-2916"],"issn":["1529-2908"]},"publication_status":"published","status":"public","article_type":"original","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"9794","department":[{"_id":"SiHi"},{"_id":"CaHe"},{"_id":"EdHa"},{"_id":"EM-Fac"},{"_id":"Bio"},{"_id":"MiSi"}],"file_date_updated":"2022-07-25T07:11:32Z","ddc":["570"],"date_updated":"2023-08-02T06:53:07Z","publisher":"Springer Nature","quality_controlled":"1","oa":1,"acknowledgement":"This research was supported by the Scientific Service Units of IST Austria through resources provided by the Imaging and Optics, Electron Microscopy, Preclinical and Life Science Facilities. We thank C. Moussion for providing anti-PNAd antibody and D. Critchley for Talin1-floxed mice, and E. Papusheva for providing a custom 3D channel alignment script. This work was supported by a European Research Council grant ERC-CoG-72437 to M.S. M.H. was supported by Czech Sciencundation GACR 20-24603Y and Charles University PRIMUS/20/MED/013.","doi":"10.1038/s41590-022-01257-4","date_published":"2022-07-11T00:00:00Z","date_created":"2021-08-06T09:09:11Z","page":"1246-1255","day":"11","publication":"Nature Immunology","has_accepted_license":"1","isi":1,"year":"2022","project":[{"grant_number":"724373","name":"Cellular navigation along spatial gradients","call_identifier":"H2020","_id":"25FE9508-B435-11E9-9278-68D0E5697425"}],"title":"Multitier mechanics control stromal adaptations in swelling lymph nodes","author":[{"full_name":"Assen, Frank P","orcid":"0000-0003-3470-6119","last_name":"Assen","first_name":"Frank P","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jun","last_name":"Abe","full_name":"Abe, Jun"},{"first_name":"Miroslav","id":"4167FE56-F248-11E8-B48F-1D18A9856A87","last_name":"Hons","orcid":"0000-0002-6625-3348","full_name":"Hons, Miroslav"},{"full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","last_name":"Hauschild","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert"},{"first_name":"Shayan","id":"40B34FE2-F248-11E8-B48F-1D18A9856A87","last_name":"Shamipour","full_name":"Shamipour, Shayan"},{"first_name":"Walter","id":"3F99E422-F248-11E8-B48F-1D18A9856A87","last_name":"Kaufmann","orcid":"0000-0001-9735-5315","full_name":"Kaufmann, Walter"},{"full_name":"Costanzo, Tommaso","orcid":"0000-0001-9732-3815","last_name":"Costanzo","id":"D93824F4-D9BA-11E9-BB12-F207E6697425","first_name":"Tommaso"},{"first_name":"Gabriel","id":"2B819732-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4761-5996","full_name":"Krens, Gabriel","last_name":"Krens"},{"id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","first_name":"Markus","last_name":"Brown","full_name":"Brown, Markus"},{"first_name":"Burkhard","last_name":"Ludewig","full_name":"Ludewig, Burkhard"},{"last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"},{"first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","last_name":"Heisenberg","orcid":"0000-0002-0912-4566","full_name":"Heisenberg, Carl-Philipp J"},{"full_name":"Weninger, Wolfgang","last_name":"Weninger","first_name":"Wolfgang"},{"id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","first_name":"Edouard B","full_name":"Hannezo, Edouard B","orcid":"0000-0001-6005-1561","last_name":"Hannezo"},{"first_name":"Sanjiv A.","last_name":"Luther","full_name":"Luther, Sanjiv A."},{"first_name":"Jens V.","full_name":"Stein, Jens V.","last_name":"Stein"},{"orcid":"0000-0002-4561-241X","full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"article_processing_charge":"No","external_id":{"isi":["000822975900002"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"short":"F.P. Assen, J. Abe, M. Hons, R. Hauschild, S. Shamipour, W. Kaufmann, T. Costanzo, G. Krens, M. Brown, B. Ludewig, S. Hippenmeyer, C.-P.J. Heisenberg, W. Weninger, E.B. Hannezo, S.A. Luther, J.V. Stein, M.K. Sixt, Nature Immunology 23 (2022) 1246–1255.","ieee":"F. P. Assen et al., “Multitier mechanics control stromal adaptations in swelling lymph nodes,” Nature Immunology, vol. 23. Springer Nature, pp. 1246–1255, 2022.","apa":"Assen, F. P., Abe, J., Hons, M., Hauschild, R., Shamipour, S., Kaufmann, W., … Sixt, M. K. (2022). Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. Springer Nature. https://doi.org/10.1038/s41590-022-01257-4","ama":"Assen FP, Abe J, Hons M, et al. Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. 2022;23:1246-1255. doi:10.1038/s41590-022-01257-4","mla":"Assen, Frank P., et al. “Multitier Mechanics Control Stromal Adaptations in Swelling Lymph Nodes.” Nature Immunology, vol. 23, Springer Nature, 2022, pp. 1246–55, doi:10.1038/s41590-022-01257-4.","ista":"Assen FP, Abe J, Hons M, Hauschild R, Shamipour S, Kaufmann W, Costanzo T, Krens G, Brown M, Ludewig B, Hippenmeyer S, Heisenberg C-PJ, Weninger W, Hannezo EB, Luther SA, Stein JV, Sixt MK. 2022. Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. 23, 1246–1255.","chicago":"Assen, Frank P, Jun Abe, Miroslav Hons, Robert Hauschild, Shayan Shamipour, Walter Kaufmann, Tommaso Costanzo, et al. “Multitier Mechanics Control Stromal Adaptations in Swelling Lymph Nodes.” Nature Immunology. Springer Nature, 2022. https://doi.org/10.1038/s41590-022-01257-4."}},{"article_number":"753","citation":{"chicago":"Cheung, Giselle T, Danijela Bataveljic, Josien Visser, Naresh Kumar, Julien Moulard, Glenn Dallérac, Daria Mozheiko, et al. “Physiological Synaptic Activity and Recognition Memory Require Astroglial Glutamine.” Nature Communications. Springer Nature, 2022. https://doi.org/10.1038/s41467-022-28331-7.","ista":"Cheung GT, Bataveljic D, Visser J, Kumar N, Moulard J, Dallérac G, Mozheiko D, Rollenhagen A, Ezan P, Mongin C, Chever O, Bemelmans AP, Lübke J, Leray I, Rouach N. 2022. Physiological synaptic activity and recognition memory require astroglial glutamine. Nature Communications. 13, 753.","mla":"Cheung, Giselle T., et al. “Physiological Synaptic Activity and Recognition Memory Require Astroglial Glutamine.” Nature Communications, vol. 13, 753, Springer Nature, 2022, doi:10.1038/s41467-022-28331-7.","apa":"Cheung, G. T., Bataveljic, D., Visser, J., Kumar, N., Moulard, J., Dallérac, G., … Rouach, N. (2022). Physiological synaptic activity and recognition memory require astroglial glutamine. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-022-28331-7","ama":"Cheung GT, Bataveljic D, Visser J, et al. Physiological synaptic activity and recognition memory require astroglial glutamine. Nature Communications. 2022;13. doi:10.1038/s41467-022-28331-7","short":"G.T. Cheung, D. Bataveljic, J. Visser, N. Kumar, J. Moulard, G. Dallérac, D. Mozheiko, A. Rollenhagen, P. Ezan, C. Mongin, O. Chever, A.P. Bemelmans, J. Lübke, I. Leray, N. Rouach, Nature Communications 13 (2022).","ieee":"G. T. Cheung et al., “Physiological synaptic activity and recognition memory require astroglial glutamine,” Nature Communications, vol. 13. Springer Nature, 2022."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","author":[{"last_name":"Cheung","full_name":"Cheung, Giselle T","id":"471195F6-F248-11E8-B48F-1D18A9856A87","first_name":"Giselle T"},{"last_name":"Bataveljic","full_name":"Bataveljic, Danijela","first_name":"Danijela"},{"first_name":"Josien","full_name":"Visser, Josien","last_name":"Visser"},{"last_name":"Kumar","full_name":"Kumar, Naresh","first_name":"Naresh"},{"last_name":"Moulard","full_name":"Moulard, Julien","first_name":"Julien"},{"full_name":"Dallérac, Glenn","last_name":"Dallérac","first_name":"Glenn"},{"first_name":"Daria","full_name":"Mozheiko, Daria","last_name":"Mozheiko"},{"full_name":"Rollenhagen, Astrid","last_name":"Rollenhagen","first_name":"Astrid"},{"first_name":"Pascal","last_name":"Ezan","full_name":"Ezan, Pascal"},{"first_name":"Cédric","full_name":"Mongin, Cédric","last_name":"Mongin"},{"last_name":"Chever","full_name":"Chever, Oana","first_name":"Oana"},{"full_name":"Bemelmans, Alexis Pierre","last_name":"Bemelmans","first_name":"Alexis Pierre"},{"full_name":"Lübke, Joachim","last_name":"Lübke","first_name":"Joachim"},{"first_name":"Isabelle","last_name":"Leray","full_name":"Leray, Isabelle"},{"last_name":"Rouach","full_name":"Rouach, Nathalie","first_name":"Nathalie"}],"article_processing_charge":"No","external_id":{"isi":["000757297200017"],"pmid":["35136061"]},"title":"Physiological synaptic activity and recognition memory require astroglial glutamine","acknowledgement":"We thank D. Mazaud and. J. Cazères for technical assistance. This work was supported by grants from the European Research Council (Consolidator grant #683154) and European Union’s Horizon 2020 research and innovation program (Marie Sklodowska-Curie Innovative Training Networks, grant #722053, EU-GliaPhD) to N.R. and from FP7-PEOPLE Marie Curie Intra-European Fellowship for career development (grant #622289) to G.C.","publisher":"Springer Nature","quality_controlled":"1","oa":1,"has_accepted_license":"1","isi":1,"year":"2022","day":"08","publication":"Nature Communications","doi":"10.1038/s41467-022-28331-7","date_published":"2022-02-08T00:00:00Z","date_created":"2022-02-20T23:01:30Z","_id":"10764","type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","date_updated":"2023-08-02T14:25:01Z","ddc":["570"],"file_date_updated":"2022-02-21T07:51:33Z","department":[{"_id":"SiHi"}],"abstract":[{"text":"Presynaptic glutamate replenishment is fundamental to brain function. In high activity regimes, such as epileptic episodes, this process is thought to rely on the glutamate-glutamine cycle between neurons and astrocytes. However the presence of an astroglial glutamine supply, as well as its functional relevance in vivo in the healthy brain remain controversial, partly due to a lack of tools that can directly examine glutamine transfer. Here, we generated a fluorescent probe that tracks glutamine in live cells, which provides direct visual evidence of an activity-dependent glutamine supply from astroglial networks to presynaptic structures under physiological conditions. This mobilization is mediated by connexin43, an astroglial protein with both gap-junction and hemichannel functions, and is essential for synaptic transmission and object recognition memory. Our findings uncover an indispensable recruitment of astroglial glutamine in physiological synaptic activity and memory via an unconventional pathway, thus providing an astrocyte basis for cognitive processes.","lang":"eng"}],"pmid":1,"oa_version":"Published Version","scopus_import":"1","month":"02","intvolume":" 13","publication_identifier":{"eissn":["20411723"]},"publication_status":"published","file":[{"creator":"dernst","date_updated":"2022-02-21T07:51:33Z","file_size":7910519,"date_created":"2022-02-21T07:51:33Z","file_name":"2022_NatureCommunications_Cheung.pdf","access_level":"open_access","relation":"main_file","content_type":"application/pdf","checksum":"51d580aff2327dd957946208a9749e1a","file_id":"10777","success":1}],"language":[{"iso":"eng"}],"volume":13},{"publication":"Molecular Autism","day":"22","year":"2022","has_accepted_license":"1","isi":1,"date_created":"2022-06-23T14:28:55Z","doi":"10.1186/s13229-022-00508-3","date_published":"2022-06-22T00:00:00Z","acknowledgement":"This study was funded by NIMH R21MH115347 to KSZ. KSZ is further supported by Shriners Hospitals for Children.\r\nWe would like to thank Angelo Harlan de Crescenzo for early contributions to this project.","oa":1,"quality_controlled":"1","publisher":"Springer Nature","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ista":"Schaaf ZA, Tat L, Cannizzaro N, Green R, Rülicke T, Hippenmeyer S, Zarbalis KS. 2022. WDFY3 mutation alters laminar position and morphology of cortical neurons. Molecular Autism. 13, 27.","chicago":"Schaaf, Zachary A., Lyvin Tat, Noemi Cannizzaro, Ralph Green, Thomas Rülicke, Simon Hippenmeyer, and Konstantinos S. Zarbalis. “WDFY3 Mutation Alters Laminar Position and Morphology of Cortical Neurons.” Molecular Autism. Springer Nature, 2022. https://doi.org/10.1186/s13229-022-00508-3.","ama":"Schaaf ZA, Tat L, Cannizzaro N, et al. WDFY3 mutation alters laminar position and morphology of cortical neurons. Molecular Autism. 2022;13. doi:10.1186/s13229-022-00508-3","apa":"Schaaf, Z. A., Tat, L., Cannizzaro, N., Green, R., Rülicke, T., Hippenmeyer, S., & Zarbalis, K. S. (2022). WDFY3 mutation alters laminar position and morphology of cortical neurons. Molecular Autism. Springer Nature. https://doi.org/10.1186/s13229-022-00508-3","ieee":"Z. A. Schaaf et al., “WDFY3 mutation alters laminar position and morphology of cortical neurons,” Molecular Autism, vol. 13. Springer Nature, 2022.","short":"Z.A. Schaaf, L. Tat, N. Cannizzaro, R. Green, T. Rülicke, S. Hippenmeyer, K.S. Zarbalis, Molecular Autism 13 (2022).","mla":"Schaaf, Zachary A., et al. “WDFY3 Mutation Alters Laminar Position and Morphology of Cortical Neurons.” Molecular Autism, vol. 13, 27, Springer Nature, 2022, doi:10.1186/s13229-022-00508-3."},"title":"WDFY3 mutation alters laminar position and morphology of cortical neurons","external_id":{"isi":["000814641400001"]},"article_processing_charge":"No","author":[{"full_name":"Schaaf, Zachary A.","last_name":"Schaaf","first_name":"Zachary A."},{"first_name":"Lyvin","full_name":"Tat, Lyvin","last_name":"Tat"},{"first_name":"Noemi","last_name":"Cannizzaro","full_name":"Cannizzaro, Noemi"},{"first_name":"Ralph","full_name":"Green, Ralph","last_name":"Green"},{"first_name":"Thomas","last_name":"Rülicke","full_name":"Rülicke, Thomas"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"},{"first_name":"Konstantinos S.","last_name":"Zarbalis","full_name":"Zarbalis, Konstantinos S."}],"article_number":"27","language":[{"iso":"eng"}],"file":[{"checksum":"525d2618e855139089bbfc3e3d49d1b2","file_id":"11461","success":1,"content_type":"application/pdf","access_level":"open_access","relation":"main_file","date_created":"2022-06-24T08:22:59Z","file_name":"2022_MolecularAutism_Schaaf.pdf","date_updated":"2022-06-24T08:22:59Z","file_size":7552298,"creator":"dernst"}],"publication_status":"published","publication_identifier":{"issn":["2040-2392"]},"related_material":{"link":[{"relation":"erratum","url":"https://doi.org/10.1186/s13229-023-00539-4"}]},"volume":13,"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Background: Proper cerebral cortical development depends on the tightly orchestrated migration of newly born neurons from the inner ventricular and subventricular zones to the outer cortical plate. Any disturbance in this process during prenatal stages may lead to neuronal migration disorders (NMDs), which can vary in extent from focal to global. Furthermore, NMDs show a substantial comorbidity with other neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous work demonstrated focal neuronal migration defects in mice carrying loss-of-function alleles of the recognized autism risk gene WDFY3. However, the cellular origins of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide critical insight into WDFY3-dependent disease pathology.\r\nMethods: Here, in an effort to untangle the origins of NMDs in Wdfy3lacZ mice, we employed mosaic analysis with double markers (MADM). MADM technology enabled us to genetically distinctly track and phenotypically analyze mutant and wild-type cells concomitantly in vivo using immunofluorescent techniques.\r\nResults: We revealed a cell autonomous requirement of WDFY3 for accurate laminar positioning of cortical projection neurons and elimination of mispositioned cells during early postnatal life. In addition, we identified significant deviations in dendritic arborization, as well as synaptic density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant neurons in Wdfy3-MADM reporter mice at postnatal stages.\r\nLimitations: While Wdfy3 mutant mice have provided valuable insight into prenatal aspects of ASD pathology that remain inaccessible to investigation in humans, like most animal models, they do not a perfectly replicate all aspects of human ASD biology. The lack of human data makes it indeterminate whether morphological deviations described here apply to ASD patients or some of the other neurodevelopmental conditions associated with WDFY3 mutation.\r\nConclusions: Our genetic approach revealed several cell autonomous requirements of WDFY3 in neuronal development that could underlie the pathogenic mechanisms of WDFY3-related neurodevelopmental conditions. The results are also consistent with findings in other ASD animal models and patients and suggest an important role for WDFY3 in regulating neuronal function and interconnectivity in postnatal life."}],"intvolume":" 13","month":"06","ddc":["570"],"date_updated":"2023-08-03T07:21:32Z","file_date_updated":"2022-06-24T08:22:59Z","department":[{"_id":"SiHi"}],"_id":"11460","keyword":["Psychiatry and Mental health","Developmental Biology","Developmental Neuroscience","Molecular Biology"],"status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"original","type":"journal_article"},{"doi":"10.1016/j.cels.2022.03.006","date_published":"2022-06-15T00:00:00Z","date_created":"2022-06-19T22:01:57Z","page":"438-453.e5","day":"15","publication":"Cell Systems","isi":1,"year":"2022","quality_controlled":"1","publisher":"Elsevier","oa":1,"acknowledgement":"D.J.A. thanks Wayne K. Potts, Alan R. Rogers, Kristen Hawkes, Ryk Ward, and Jon Seger for inspiring a young undergraduate to apply evolutionary theory to intraorganism development. Supported by the Paul G. Allen Frontiers Group (University of Washington); NIH R00HG010152 (Dartmouth); and NÖ Forschung und Bildung n[f+b] life science call grant (C13-002) and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program 725780 LinPro to S.H.","title":"Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development","author":[{"first_name":"Donovan J.","full_name":"Anderson, Donovan J.","last_name":"Anderson"},{"full_name":"Pauler, Florian","last_name":"Pauler","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","first_name":"Florian"},{"first_name":"Aaron","last_name":"Mckenna","full_name":"Mckenna, Aaron"},{"first_name":"Jay","full_name":"Shendure, Jay","last_name":"Shendure"},{"last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Horwitz","full_name":"Horwitz, Marshall S.","first_name":"Marshall S."}],"external_id":{"pmid":["35452605"],"isi":["000814124400002"]},"article_processing_charge":"No","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"chicago":"Anderson, Donovan J., Florian Pauler, Aaron Mckenna, Jay Shendure, Simon Hippenmeyer, and Marshall S. Horwitz. “Simultaneous Brain Cell Type and Lineage Determined by ScRNA-Seq Reveals Stereotyped Cortical Development.” Cell Systems. Elsevier, 2022. https://doi.org/10.1016/j.cels.2022.03.006.","ista":"Anderson DJ, Pauler F, Mckenna A, Shendure J, Hippenmeyer S, Horwitz MS. 2022. Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development. Cell Systems. 13(6), 438–453.e5.","mla":"Anderson, Donovan J., et al. “Simultaneous Brain Cell Type and Lineage Determined by ScRNA-Seq Reveals Stereotyped Cortical Development.” Cell Systems, vol. 13, no. 6, Elsevier, 2022, p. 438–453.e5, doi:10.1016/j.cels.2022.03.006.","short":"D.J. Anderson, F. Pauler, A. Mckenna, J. Shendure, S. Hippenmeyer, M.S. Horwitz, Cell Systems 13 (2022) 438–453.e5.","ieee":"D. J. Anderson, F. Pauler, A. Mckenna, J. Shendure, S. Hippenmeyer, and M. S. Horwitz, “Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development,” Cell Systems, vol. 13, no. 6. Elsevier, p. 438–453.e5, 2022.","apa":"Anderson, D. J., Pauler, F., Mckenna, A., Shendure, J., Hippenmeyer, S., & Horwitz, M. S. (2022). Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development. Cell Systems. Elsevier. https://doi.org/10.1016/j.cels.2022.03.006","ama":"Anderson DJ, Pauler F, Mckenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development. Cell Systems. 2022;13(6):438-453.e5. doi:10.1016/j.cels.2022.03.006"},"project":[{"call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780"},{"_id":"25D92700-B435-11E9-9278-68D0E5697425","grant_number":"LS13-002","name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain"}],"volume":13,"issue":"6","ec_funded":1,"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2405-4712"],"eissn":["2405-4720"]},"publication_status":"published","month":"06","intvolume":" 13","scopus_import":"1","main_file_link":[{"url":"https://doi.org/10.1016/j.cels.2022.03.006","open_access":"1"}],"oa_version":"Published Version","pmid":1,"abstract":[{"lang":"eng","text":"Mutations are acquired frequently, such that each cell's genome inscribes its history of cell divisions. Common genomic alterations involve loss of heterozygosity (LOH). LOH accumulates throughout the genome, offering large encoding capacity for inferring cell lineage. Using only single-cell RNA sequencing (scRNA-seq) of mouse brain cells, we found that LOH events spanning multiple genes are revealed as tracts of monoallelically expressed, constitutionally heterozygous single-nucleotide variants (SNVs). We simultaneously inferred cell lineage and marked developmental time points based on X chromosome inactivation and the total number of LOH events while identifying cell types from gene expression patterns. Our results are consistent with progenitor cells giving rise to multiple cortical cell types through stereotyped expansion and distinct waves of neurogenesis. This type of retrospective analysis could be incorporated into scRNA-seq pipelines and, compared with experimental approaches for determining lineage in model organisms, is applicable where genetic engineering is prohibited, such as humans."}],"department":[{"_id":"SiHi"}],"date_updated":"2023-08-03T07:19:43Z","status":"public","type":"journal_article","article_type":"original","_id":"11449"},{"date_created":"2023-01-16T10:03:24Z","doi":"10.1242/jcs.259234","date_published":"2022-04-01T00:00:00Z","publication":"Journal of Cell Science","day":"01","year":"2022","isi":1,"has_accepted_license":"1","oa":1,"publisher":"The Company of Biologists","quality_controlled":"1","acknowledgement":"J.A. was supported by a grant from the Medical Research Council (MRC), UK (MR/R000352/1) to C.A.M. Cryo-EM data were collected on equipment funded by the Wellcome Trust, UK (079605/Z/06/Z) and the Biotechnology and Biological Sciences Research Council (BBSRC) UK (BB/L014211/1). F.F.’s salary and institute were supported by Inserm (Institut National de la Santé et de la Recherche Médicale), CNRS (Centre National de la Recherche Scientifique) and Sorbonne Université. F.F.’s group was particularly supported by Agence Nationale de la\r\nRecherche (ANR-16-CE16-0011-03) and Seventh Framework Programme (EUHEALTH-\r\n2013, DESIRE, N° 60253; also funding M.S.’s salary) and the European Cooperation in Science and Technology (COST Action CA16118). Open Access funding provided by Birkbeck College: Birkbeck University of London. Deposited in PMC for immediate release.","title":"Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography","external_id":{"pmid":["35383828"],"isi":["000783840400010"]},"article_processing_charge":"No","author":[{"last_name":"Atherton","full_name":"Atherton, Joseph","first_name":"Joseph"},{"last_name":"Stouffer","full_name":"Stouffer, Melissa A","id":"4C9372C4-F248-11E8-B48F-1D18A9856A87","first_name":"Melissa A"},{"first_name":"Fiona","full_name":"Francis, Fiona","last_name":"Francis"},{"first_name":"Carolyn A.","last_name":"Moores","full_name":"Moores, Carolyn A."}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"chicago":"Atherton, Joseph, Melissa A Stouffer, Fiona Francis, and Carolyn A. Moores. “Visualising the Cytoskeletal Machinery in Neuronal Growth Cones Using Cryo-Electron Tomography.” Journal of Cell Science. The Company of Biologists, 2022. https://doi.org/10.1242/jcs.259234.","ista":"Atherton J, Stouffer MA, Francis F, Moores CA. 2022. Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography. Journal of Cell Science. 135(7), 259234.","mla":"Atherton, Joseph, et al. “Visualising the Cytoskeletal Machinery in Neuronal Growth Cones Using Cryo-Electron Tomography.” Journal of Cell Science, vol. 135, no. 7, 259234, The Company of Biologists, 2022, doi:10.1242/jcs.259234.","apa":"Atherton, J., Stouffer, M. A., Francis, F., & Moores, C. A. (2022). Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography. Journal of Cell Science. The Company of Biologists. https://doi.org/10.1242/jcs.259234","ama":"Atherton J, Stouffer MA, Francis F, Moores CA. Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography. Journal of Cell Science. 2022;135(7). doi:10.1242/jcs.259234","ieee":"J. Atherton, M. A. Stouffer, F. Francis, and C. A. Moores, “Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography,” Journal of Cell Science, vol. 135, no. 7. The Company of Biologists, 2022.","short":"J. Atherton, M.A. Stouffer, F. Francis, C.A. Moores, Journal of Cell Science 135 (2022)."},"article_number":"259234","volume":135,"issue":"7","language":[{"iso":"eng"}],"file":[{"success":1,"file_id":"12461","checksum":"4346ed32cb7c89a8ca051c7da68a9a1c","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_name":"2022_JourCellBiology_Atherton.pdf","date_created":"2023-01-30T11:41:01Z","file_size":13868733,"date_updated":"2023-01-30T11:41:01Z","creator":"dernst"}],"publication_status":"published","publication_identifier":{"eissn":["1477-9137"],"issn":["0021-9533"]},"intvolume":" 135","month":"04","scopus_import":"1","pmid":1,"oa_version":"Published Version","abstract":[{"text":"Neurons extend axons to form the complex circuitry of the mature brain. This depends on the coordinated response and continuous remodelling of the microtubule and F-actin networks in the axonal growth cone. Growth cone architecture remains poorly understood at nanoscales. We therefore investigated mouse hippocampal neuron growth cones using cryo-electron tomography to directly visualise their three-dimensional subcellular architecture with molecular detail. Our data showed that the hexagonal arrays of actin bundles that form filopodia penetrate and terminate deep within the growth cone interior. We directly observed the modulation of these and other growth cone actin bundles by alteration of individual F-actin helical structures. Microtubules with blunt, slightly flared or gently curved ends predominated in the growth cone, frequently contained lumenal particles and exhibited lattice defects. Investigation of the effect of absence of doublecortin, a neurodevelopmental cytoskeleton regulator, on growth cone cytoskeleton showed no major anomalies in overall growth cone organisation or in F-actin subpopulations. However, our data suggested that microtubules sustained more structural defects, highlighting the importance of microtubule integrity during growth cone migration.","lang":"eng"}],"file_date_updated":"2023-01-30T11:41:01Z","department":[{"_id":"SiHi"}],"ddc":["570"],"date_updated":"2023-08-04T10:28:34Z","keyword":["Cell Biology"],"status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","_id":"12283"},{"_id":"12282","type":"journal_article","article_type":"letter_note","status":"public","date_updated":"2023-08-04T10:28:04Z","department":[{"_id":"SiHi"},{"_id":"LeSa"}],"abstract":[{"lang":"eng","text":"From a simple thought to a multicellular movement"}],"pmid":1,"oa_version":"None","scopus_import":"1","month":"04","intvolume":" 135","publication_identifier":{"issn":["0021-9533"],"eissn":["1477-9137"]},"publication_status":"published","language":[{"iso":"eng"}],"volume":135,"issue":"8","article_number":"260017","citation":{"chicago":"Amberg, Nicole, Melissa A Stouffer, and Irene Vercellino. “Operation STEM Fatale – How an Equity, Diversity and Inclusion Initiative Has Brought Us to Reflect on the Current Challenges in Cell Biology and Science as a Whole.” Journal of Cell Science. The Company of Biologists, 2022. https://doi.org/10.1242/jcs.260017.","ista":"Amberg N, Stouffer MA, Vercellino I. 2022. Operation STEM fatale – how an equity, diversity and inclusion initiative has brought us to reflect on the current challenges in cell biology and science as a whole. Journal of Cell Science. 135(8), 260017.","mla":"Amberg, Nicole, et al. “Operation STEM Fatale – How an Equity, Diversity and Inclusion Initiative Has Brought Us to Reflect on the Current Challenges in Cell Biology and Science as a Whole.” Journal of Cell Science, vol. 135, no. 8, 260017, The Company of Biologists, 2022, doi:10.1242/jcs.260017.","ama":"Amberg N, Stouffer MA, Vercellino I. Operation STEM fatale – how an equity, diversity and inclusion initiative has brought us to reflect on the current challenges in cell biology and science as a whole. Journal of Cell Science. 2022;135(8). doi:10.1242/jcs.260017","apa":"Amberg, N., Stouffer, M. A., & Vercellino, I. (2022). Operation STEM fatale – how an equity, diversity and inclusion initiative has brought us to reflect on the current challenges in cell biology and science as a whole. Journal of Cell Science. The Company of Biologists. https://doi.org/10.1242/jcs.260017","ieee":"N. Amberg, M. A. Stouffer, and I. Vercellino, “Operation STEM fatale – how an equity, diversity and inclusion initiative has brought us to reflect on the current challenges in cell biology and science as a whole,” Journal of Cell Science, vol. 135, no. 8. The Company of Biologists, 2022.","short":"N. Amberg, M.A. Stouffer, I. Vercellino, Journal of Cell Science 135 (2022)."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","author":[{"first_name":"Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","last_name":"Amberg","full_name":"Amberg, Nicole","orcid":"0000-0002-3183-8207"},{"full_name":"Stouffer, Melissa A","last_name":"Stouffer","first_name":"Melissa A","id":"4C9372C4-F248-11E8-B48F-1D18A9856A87"},{"id":"3ED6AF16-F248-11E8-B48F-1D18A9856A87","first_name":"Irene","last_name":"Vercellino","orcid":"0000-0001-5618-3449","full_name":"Vercellino, Irene"}],"article_processing_charge":"No","external_id":{"isi":["000798123600015"],"pmid":["35438168"]},"title":"Operation STEM fatale – how an equity, diversity and inclusion initiative has brought us to reflect on the current challenges in cell biology and science as a whole","acknowledgement":"The authors want to thank Professors Carrie Bernecky, Tom Henzinger, Martin Loose and Gaia Novarino for accepting to be interviewed, thus giving significant contribution to the discussion that lead to this article.","quality_controlled":"1","publisher":"The Company of Biologists","isi":1,"year":"2022","day":"19","publication":"Journal of Cell Science","doi":"10.1242/jcs.260017","date_published":"2022-04-19T00:00:00Z","date_created":"2023-01-16T10:03:14Z"},{"abstract":[{"text":"Background\r\nProper cerebral cortical development depends on the tightly orchestrated migration of newly born neurons from the inner ventricular and subventricular zones to the outer cortical plate. Any disturbance in this process during prenatal stages may lead to neuronal migration disorders (NMDs), which can vary in extent from focal to global. Furthermore, NMDs show a substantial comorbidity with other neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous work demonstrated focal neuronal migration defects in mice carrying loss-of-function alleles of the recognized autism risk gene WDFY3. However, the cellular origins of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide critical insight into WDFY3-dependent disease pathology .\r\nMethods\r\nHere, in an effort to untangle the origins of NMDs in Wdfy3lacZ mice, we employed mosaic analysis with double markers (MADM). MADM technology enabled us to genetically distinctly track and phenotypically analyze mutant and wild type cells concomitantly in vivo using immunofluorescent techniques.\r\nResults\r\nWe revealed a cell autonomous requirement of WDFY3 for accurate laminar positioning of cortical projection neurons and elimination of mispositioned cells during early postnatal life. In addition, we identified significant deviations in dendritic arborization, as well as synaptic density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant neurons in Wdfy3-MADM reporter mice at postnatal stages. Limitations While Wdfy3 mutant mice have provided valuable insight into prenatal aspects of ASD pathology that remain inaccessible to investigation in humans, like most animal models, they do not a perfectly replicate all aspects of human ASD biology. The lack of human data makes it indeterminate whether morphological deviations described here apply to ASD patients.\r\nConclusions\r\nOur genetic approach revealed several cell autonomous requirements of Wdfy3 in neuronal development that could underly the pathogenic mechanisms of WDFY3-related ASD conditions. The results are also consistent with findings in other ASD animal models and patients and suggest an important role for Wdfy3 in regulating neuronal function and interconnectivity in postnatal life.","lang":"eng"}],"pmid":1,"oa_version":"Preprint","publisher":"Research Square","oa":1,"main_file_link":[{"open_access":"1","url":"https://doi.org/10.21203/rs.3.rs-1316167/v1"}],"month":"02","publication_identifier":{"eissn":["2693-5015"]},"year":"2022","publication_status":"submitted","day":"16","language":[{"iso":"eng"}],"page":"30","date_published":"2022-02-16T00:00:00Z","doi":"10.21203/rs.3.rs-1316167/v1","date_created":"2022-02-25T07:53:26Z","_id":"10792","type":"preprint","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","citation":{"ama":"Schaaf Z, Tat L, Cannizzaro N, et al. WDFY3 cell autonomously controls neuronal migration. doi:10.21203/rs.3.rs-1316167/v1","apa":"Schaaf, Z., Tat, L., Cannizzaro, N., Green, R., Rülicke, T., Hippenmeyer, S., & Zarbalis, K. (n.d.). WDFY3 cell autonomously controls neuronal migration. Research Square. https://doi.org/10.21203/rs.3.rs-1316167/v1","ieee":"Z. Schaaf et al., “WDFY3 cell autonomously controls neuronal migration.” Research Square.","short":"Z. Schaaf, L. Tat, N. Cannizzaro, R. Green, T. Rülicke, S. Hippenmeyer, K. Zarbalis, (n.d.).","mla":"Schaaf, Zachary, et al. WDFY3 Cell Autonomously Controls Neuronal Migration. Research Square, doi:10.21203/rs.3.rs-1316167/v1.","ista":"Schaaf Z, Tat L, Cannizzaro N, Green R, Rülicke T, Hippenmeyer S, Zarbalis K. WDFY3 cell autonomously controls neuronal migration. 10.21203/rs.3.rs-1316167/v1.","chicago":"Schaaf, Zachary, Lyvin Tat, Noemi Cannizzaro, Ralph Green, Thomas Rülicke, Simon Hippenmeyer, and K Zarbalis. “WDFY3 Cell Autonomously Controls Neuronal Migration.” Research Square, n.d. https://doi.org/10.21203/rs.3.rs-1316167/v1."},"date_updated":"2023-10-17T13:06:52Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"first_name":"Zachary","full_name":"Schaaf, Zachary","last_name":"Schaaf"},{"full_name":"Tat, Lyvin","last_name":"Tat","first_name":"Lyvin"},{"last_name":"Cannizzaro","full_name":"Cannizzaro, Noemi","first_name":"Noemi"},{"first_name":"Ralph","last_name":"Green","full_name":"Green, Ralph"},{"last_name":"Rülicke","full_name":"Rülicke, Thomas","first_name":"Thomas"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061"},{"full_name":"Zarbalis, K","last_name":"Zarbalis","first_name":"K"}],"article_processing_charge":"No","external_id":{"pmid":["PPR454733"]},"department":[{"_id":"SiHi"}],"title":"WDFY3 cell autonomously controls neuronal migration"},{"citation":{"chicago":"Hansen, Andi H, Florian Pauler, Michael Riedl, Carmen Streicher, Anna-Magdalena Heger, Susanne Laukoter, Christoph M Sommer, et al. “Tissue-Wide Effects Override Cell-Intrinsic Gene Function in Radial Neuron Migration.” Oxford Open Neuroscience. Oxford Academic, 2022. https://doi.org/10.1093/oons/kvac009.","ista":"Hansen AH, Pauler F, Riedl M, Streicher C, Heger A-M, Laukoter S, Sommer CM, Nicolas A, Hof B, Tsai LH, Rülicke T, Hippenmeyer S. 2022. Tissue-wide effects override cell-intrinsic gene function in radial neuron migration. Oxford Open Neuroscience. 1(1), kvac009.","mla":"Hansen, Andi H., et al. “Tissue-Wide Effects Override Cell-Intrinsic Gene Function in Radial Neuron Migration.” Oxford Open Neuroscience, vol. 1, no. 1, kvac009, Oxford Academic, 2022, doi:10.1093/oons/kvac009.","ieee":"A. H. Hansen et al., “Tissue-wide effects override cell-intrinsic gene function in radial neuron migration,” Oxford Open Neuroscience, vol. 1, no. 1. Oxford Academic, 2022.","short":"A.H. Hansen, F. Pauler, M. Riedl, C. Streicher, A.-M. Heger, S. Laukoter, C.M. Sommer, A. Nicolas, B. Hof, L.H. Tsai, T. Rülicke, S. Hippenmeyer, Oxford Open Neuroscience 1 (2022).","apa":"Hansen, A. H., Pauler, F., Riedl, M., Streicher, C., Heger, A.-M., Laukoter, S., … Hippenmeyer, S. (2022). Tissue-wide effects override cell-intrinsic gene function in radial neuron migration. Oxford Open Neuroscience. Oxford Academic. https://doi.org/10.1093/oons/kvac009","ama":"Hansen AH, Pauler F, Riedl M, et al. Tissue-wide effects override cell-intrinsic gene function in radial neuron migration. Oxford Open Neuroscience. 2022;1(1). doi:10.1093/oons/kvac009"},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"id":"38853E16-F248-11E8-B48F-1D18A9856A87","first_name":"Andi H","full_name":"Hansen, Andi H","last_name":"Hansen"},{"last_name":"Pauler","orcid":"0000-0002-7462-0048","full_name":"Pauler, Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","first_name":"Florian"},{"id":"3BE60946-F248-11E8-B48F-1D18A9856A87","first_name":"Michael","orcid":"0000-0003-4844-6311","full_name":"Riedl, Michael","last_name":"Riedl"},{"full_name":"Streicher, Carmen","last_name":"Streicher","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","first_name":"Carmen"},{"last_name":"Heger","full_name":"Heger, Anna-Magdalena","first_name":"Anna-Magdalena","id":"4B76FFD2-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Susanne","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","last_name":"Laukoter","orcid":"0000-0002-7903-3010","full_name":"Laukoter, Susanne"},{"orcid":"0000-0003-1216-9105","full_name":"Sommer, Christoph M","last_name":"Sommer","first_name":"Christoph M","id":"4DF26D8C-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Nicolas, Armel","last_name":"Nicolas","id":"2A103192-F248-11E8-B48F-1D18A9856A87","first_name":"Armel"},{"first_name":"Björn","id":"3A374330-F248-11E8-B48F-1D18A9856A87","last_name":"Hof","full_name":"Hof, Björn","orcid":"0000-0003-2057-2754"},{"full_name":"Tsai, Li Huei","last_name":"Tsai","first_name":"Li Huei"},{"first_name":"Thomas","full_name":"Rülicke, Thomas","last_name":"Rülicke"},{"last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"article_processing_charge":"No","title":"Tissue-wide effects override cell-intrinsic gene function in radial neuron migration","article_number":"kvac009","project":[{"name":"Molecular Mechanisms of Cerebral Cortex Development","grant_number":"618444","call_identifier":"FP7","_id":"25D61E48-B435-11E9-9278-68D0E5697425"},{"_id":"2625A13E-B435-11E9-9278-68D0E5697425","name":"Molecular Mechanisms of Radial Neuronal Migration","grant_number":"24812"}],"has_accepted_license":"1","year":"2022","day":"07","publication":"Oxford Open Neuroscience","date_published":"2022-07-07T00:00:00Z","doi":"10.1093/oons/kvac009","date_created":"2022-02-25T07:52:11Z","acknowledgement":"A.H.H. was a recipient of a DOC Fellowship (24812) of the Austrian Academy of Sciences. This work also received support from IST Austria institutional funds; the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007–2013) under REA grant agreement No 618444 to S.H.\r\nAPC funding was obtained by IST Austria institutional funds.\r\nWe thank A. Sommer and C. Czepe (VBCF GmbH, NGS Unit), L. Andersen, J. Sonntag and J. Renno for technical support and/or initial experiments; M. Sixt, J. Nimpf and all members of the Hippenmeyer lab for discussion. This research was supported by the Scientific Service Units of IST Austria through resources provided by the Imaging and Optics Facility, Lab Support Facility and Preclinical Facility.","quality_controlled":"1","publisher":"Oxford Academic","oa":1,"date_updated":"2023-11-30T10:55:12Z","ddc":["570"],"file_date_updated":"2023-08-16T08:00:30Z","department":[{"_id":"SiHi"},{"_id":"BjHo"},{"_id":"LifeSc"},{"_id":"EM-Fac"}],"_id":"10791","article_type":"original","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","publication_identifier":{"eissn":["2753-149X"]},"publication_status":"published","file":[{"file_size":4846551,"date_updated":"2023-08-16T08:00:30Z","creator":"dernst","file_name":"2023_OxfordOpenNeuroscience_Hansen.pdf","date_created":"2023-08-16T08:00:30Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","success":1,"file_id":"14061","checksum":"822e76e056c07099d1fb27d1ece5941b"}],"language":[{"iso":"eng"}],"issue":"1","related_material":{"record":[{"status":"public","id":"12726","relation":"dissertation_contains"},{"relation":"dissertation_contains","id":"14530","status":"public"}]},"volume":1,"ec_funded":1,"abstract":[{"text":"The mammalian neocortex is composed of diverse neuronal and glial cell classes that broadly arrange in six distinct laminae. Cortical layers emerge during development and defects in the developmental programs that orchestrate cortical lamination are associated with neurodevelopmental diseases. The developmental principle of cortical layer formation depends on concerted radial projection neuron migration, from their birthplace to their final target position. Radial migration occurs in defined sequential steps, regulated by a large array of signaling pathways. However, based on genetic loss-of-function experiments, most studies have thus far focused on the role of cell-autonomous gene function. Yet, cortical neuron migration in situ is a complex process and migrating neurons traverse along diverse cellular compartments and environments. The role of tissue-wide properties and genetic state in radial neuron migration is however not clear. Here we utilized mosaic analysis with double markers (MADM) technology to either sparsely or globally delete gene function, followed by quantitative single-cell phenotyping. The MADM-based gene ablation paradigms in combination with computational modeling demonstrated that global tissue-wide effects predominate cell-autonomous gene function albeit in a gene-specific manner. Our results thus suggest that the genetic landscape in a tissue critically affects the overall migration phenotype of individual cortical projection neurons. In a broader context, our findings imply that global tissue-wide effects represent an essential component of the underlying etiology associated with focal malformations of cortical development in particular, and neurological diseases in general.","lang":"eng"}],"acknowledged_ssus":[{"_id":"LifeSc"},{"_id":"PreCl"},{"_id":"Bio"}],"oa_version":"Published Version","month":"07","intvolume":" 1"},{"date_published":"2021-01-01T00:00:00Z","doi":"10.1101/2020.12.31.425016","date_created":"2021-02-04T07:23:23Z","ec_funded":1,"year":"2021","publication_status":"submitted","day":"01","language":[{"iso":"eng"}],"publication":"bioRxiv","publisher":"Cold Spring Harbor Laboratory","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/2020.12.31.425016"}],"oa":1,"month":"01","abstract":[{"text":"Acquired mutations are sufficiently frequent such that the genome of a single cell offers a record of its history of cell divisions. Among more common somatic genomic alterations are loss of heterozygosity (LOH). Large LOH events are potentially detectable in single cell RNA sequencing (scRNA-seq) datasets as tracts of monoallelic expression for constitutionally heterozygous single nucleotide variants (SNVs) located among contiguous genes. We identified runs of monoallelic expression, consistent with LOH, uniquely distributed throughout the genome in single cell brain cortex transcriptomes of F1 hybrids involving different inbred mouse strains. We then phylogenetically reconstructed single cell lineages and simultaneously identified cell types by corresponding gene expression patterns. Our results are consistent with progenitor cells giving rise to multiple cortical cell types through stereotyped expansion and distinct waves of neurogenesis. Compared to engineered recording systems, LOH events accumulate throughout the genome and across the lifetime of an organism, affording tremendous capacity for encoding lineage information and increasing resolution for later cell divisions. This approach can conceivably be computationally incorporated into scRNA-seq analysis and may be useful for organisms where genetic engineering is prohibitive, such as humans.","lang":"eng"}],"oa_version":"Preprint","acknowledgement":"We thank Bill Bolosky, Microsoft Research, for earlier work showing proof of concept in TCGA\r\nbulk RNA-seq data. Supported by the Paul G. Allen Frontiers Group (University of Washington);\r\nNIH R00HG010152 (Dartmouth); and NÖ Forschung und Bildung n[f+b] life science call grant\r\n(C13-002) to SH, and the European Research Council (ERC) under the European Union’s\r\nHorizon 2020 research and innovation program 725780 LinPro to SH.","author":[{"first_name":"Donovan J.","full_name":"Anderson, Donovan J.","last_name":"Anderson"},{"id":"48EA0138-F248-11E8-B48F-1D18A9856A87","first_name":"Florian","full_name":"Pauler, Florian","last_name":"Pauler"},{"first_name":"Aaron","full_name":"McKenna, Aaron","last_name":"McKenna"},{"last_name":"Shendure","full_name":"Shendure, Jay","first_name":"Jay"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"},{"first_name":"Marshall S.","full_name":"Horwitz, Marshall S.","last_name":"Horwitz"}],"article_processing_charge":"No","department":[{"_id":"SiHi"}],"title":"Simultaneous identification of brain cell type and lineage via single cell RNA sequencing","date_updated":"2021-02-04T07:29:53Z","citation":{"ista":"Anderson DJ, Pauler F, McKenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous identification of brain cell type and lineage via single cell RNA sequencing. bioRxiv, 10.1101/2020.12.31.425016.","chicago":"Anderson, Donovan J., Florian Pauler, Aaron McKenna, Jay Shendure, Simon Hippenmeyer, and Marshall S. Horwitz. “Simultaneous Identification of Brain Cell Type and Lineage via Single Cell RNA Sequencing.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2020.12.31.425016.","apa":"Anderson, D. J., Pauler, F., McKenna, A., Shendure, J., Hippenmeyer, S., & Horwitz, M. S. (n.d.). Simultaneous identification of brain cell type and lineage via single cell RNA sequencing. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2020.12.31.425016","ama":"Anderson DJ, Pauler F, McKenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous identification of brain cell type and lineage via single cell RNA sequencing. bioRxiv. doi:10.1101/2020.12.31.425016","ieee":"D. J. Anderson, F. Pauler, A. McKenna, J. Shendure, S. Hippenmeyer, and M. S. Horwitz, “Simultaneous identification of brain cell type and lineage via single cell RNA sequencing,” bioRxiv. Cold Spring Harbor Laboratory.","short":"D.J. Anderson, F. Pauler, A. McKenna, J. Shendure, S. Hippenmeyer, M.S. Horwitz, BioRxiv (n.d.).","mla":"Anderson, Donovan J., et al. “Simultaneous Identification of Brain Cell Type and Lineage via Single Cell RNA Sequencing.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2020.12.31.425016."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","type":"preprint","project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}],"status":"public","_id":"9082"},{"title":"Identification of neural oscillations and epileptiform changes in human brain organoids","article_processing_charge":"Yes","external_id":{"pmid":["34426698 "],"isi":["000687516300001"]},"author":[{"last_name":"Samarasinghe","full_name":"Samarasinghe, Ranmal A.","first_name":"Ranmal A."},{"full_name":"Miranda, Osvaldo","orcid":"0000-0001-6618-6889","last_name":"Miranda","first_name":"Osvaldo","id":"862A3C56-A8BF-11E9-B4FA-D9E3E5697425"},{"first_name":"Jessie E.","full_name":"Buth, Jessie E.","last_name":"Buth"},{"first_name":"Simon","last_name":"Mitchell","full_name":"Mitchell, Simon"},{"first_name":"Isabella","last_name":"Ferando","full_name":"Ferando, Isabella"},{"first_name":"Momoko","full_name":"Watanabe, Momoko","last_name":"Watanabe"},{"last_name":"Kurdian","full_name":"Kurdian, Arinnae","first_name":"Arinnae"},{"full_name":"Golshani, Peyman","last_name":"Golshani","first_name":"Peyman"},{"full_name":"Plath, Kathrin","last_name":"Plath","first_name":"Kathrin"},{"last_name":"Lowry","full_name":"Lowry, William E.","first_name":"William E."},{"first_name":"Jack M.","last_name":"Parent","full_name":"Parent, Jack M."},{"full_name":"Mody, Istvan","last_name":"Mody","first_name":"Istvan"},{"first_name":"Bennett G.","full_name":"Novitch, Bennett G.","last_name":"Novitch"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ama":"Samarasinghe RA, Miranda O, Buth JE, et al. Identification of Neural Oscillations and Epileptiform Changes in Human Brain Organoids. Vol 24. Springer Nature; 2021. doi:10.1038/s41593-021-00906-5","apa":"Samarasinghe, R. A., Miranda, O., Buth, J. E., Mitchell, S., Ferando, I., Watanabe, M., … Novitch, B. G. (2021). Identification of neural oscillations and epileptiform changes in human brain organoids (Vol. 24). Springer Nature. https://doi.org/10.1038/s41593-021-00906-5","short":"R.A. Samarasinghe, O. Miranda, J.E. Buth, S. Mitchell, I. Ferando, M. Watanabe, A. Kurdian, P. Golshani, K. Plath, W.E. Lowry, J.M. Parent, I. Mody, B.G. Novitch, Identification of Neural Oscillations and Epileptiform Changes in Human Brain Organoids, Springer Nature, 2021.","ieee":"R. A. Samarasinghe et al., Identification of neural oscillations and epileptiform changes in human brain organoids, vol. 24. Springer Nature, 2021.","mla":"Samarasinghe, Ranmal A., et al. Identification of Neural Oscillations and Epileptiform Changes in Human Brain Organoids. Vol. 24, Springer Nature, 2021, doi:10.1038/s41593-021-00906-5.","ista":"Samarasinghe RA, Miranda O, Buth JE, Mitchell S, Ferando I, Watanabe M, Kurdian A, Golshani P, Plath K, Lowry WE, Parent JM, Mody I, Novitch BG. 2021. Identification of neural oscillations and epileptiform changes in human brain organoids, Springer Nature, 32p.","chicago":"Samarasinghe, Ranmal A., Osvaldo Miranda, Jessie E. Buth, Simon Mitchell, Isabella Ferando, Momoko Watanabe, Arinnae Kurdian, et al. Identification of Neural Oscillations and Epileptiform Changes in Human Brain Organoids. Vol. 24. Springer Nature, 2021. https://doi.org/10.1038/s41593-021-00906-5."},"date_created":"2019-11-10T11:23:58Z","doi":"10.1038/s41593-021-00906-5","date_published":"2021-08-23T00:00:00Z","page":"32","day":"23","year":"2021","isi":1,"oa":1,"publisher":"Springer Nature","acknowledgement":"We thank S. Butler, T. Carmichael and members of the laboratory of B.G.N. for helpful discussions and comments on the manuscript; N. Vishlaghi and F. Turcios-Hernandez for technical assistance, and J. Lee, S.-K. Lee, H. Shinagawa and K. Yoshikawa for valuable reagents. We also thank the UCLA Eli and Edythe Broad Stem Cell Research Center (BSCRC) and Intellectual and Developmental Disabilities Research Center microscopy cores for access to imaging facilities. This work was supported by grants from the California Institute for Regenerative Medicine (CIRM) (DISC1-08819 to B.G.N.), the National Institute of Health (R01NS089817, R01DA051897 and P50HD103557 to B.G.N.; K08NS119747 to R.A.S.; K99HD096105 to M.W.; R01MH123922, R01MH121521 and P50HD103557 to M.J.G.; R01GM099134 to K.P.; R01NS103788 to W.E.L.; R01NS088571 to J.M.P.; R01NS030549 and R01AG050474 to I.M.), and research awards from the UCLA Jonsson Comprehensive Cancer Center and BSCRC Ablon Scholars Program (to B.G.N.), the BSCRC Innovation Program (to B.G.N., K.P. and W.E.L.), the UCLA BSCRC Steffy Brain Aging Research Fund (to B.G.N. and W.E.L.) and the UCLA Clinical and Translational Science Institute (to B.G.N.), Paul Allen Family Foundation Frontiers Group (to K.P. and W.E.L.), the March of Dimes Foundation (to W.E.L.) and the Simons Foundation Autism Research Initiative Bridge to Independence Program (to R.A.S. and M.J.G.). R.A.S. was also supported by the UCLA/NINDS Translational Neuroscience Training Grant (R25NS065723), a Research and Training Fellowship from the American Epilepsy Society, a Taking Flight Award from CURE Epilepsy and a Clinician Scientist training award from the UCLA BSCRC. J.E.B. was supported by the UCLA BSCRC Rose Hills Foundation Graduate Scholarship Training Program. M.W. was supported by postdoctoral training awards provided by the UCLA BSCRC and the Uehara Memorial Foundation. O.A.M. and A.K. were supported in part by the UCLA-California State University Northridge CIRM-Bridges training program (EDUC2-08411). We also acknowledge the support of the IDDRC Cells, Circuits and Systems Analysis, Microscopy and Genetics and Genomics Cores of the Semel Institute of Neuroscience at UCLA, which are supported by the NICHD (U54HD087101 and P50HD10355701). We lastly acknowledge support from a Quantitative and Computational Biosciences Collaboratory Postdoctoral Fellowship to S.M. and the Quantitative and Computational Biosciences Collaboratory community, directed by M. Pellegrini.","department":[{"_id":"GradSch"},{"_id":"SiHi"}],"date_updated":"2023-08-04T10:49:44Z","status":"public","type":"technical_report","_id":"6995","volume":24,"language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"eissn":["1546-1726"],"issn":["1097-6256"]},"intvolume":" 24","month":"08","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1038/s41593-021-00906-5"}],"alternative_title":["Nature Neuroscience"],"oa_version":"Published Version","pmid":1,"abstract":[{"lang":"eng","text":"Human brain organoids represent a powerful tool for the study of human neurological diseases particularly those that impact brain growth and structure. However, many neurological diseases lack obvious anatomical abnormalities, yet significantly impact neural network functions, raising the question of whether organoids possess sufficient neural network architecture and complexity to model these conditions. Here, we explore the network level functions of brain organoids using calcium sensor imaging and extracellular recording approaches that together reveal the existence of complex oscillatory network behaviors reminiscent of intact brain preparations. We further demonstrate strikingly abnormal epileptiform network activity in organoids derived from a Rett Syndrome patient despite only modest anatomical differences from isogenically matched controls, and rescue with an unconventional neuromodulatory drug Pifithrin-α. Together, these findings provide an essential foundation for the utilization of human brain organoids to study intact and disordered human brain network formation and illustrate their utility in therapeutic discovery."}]},{"acknowledgement":"This work was supported by the program “Investissements d’avenir” ANR-10-IAIHU-06 , ICM , a Sorbonne Université Emergence grant, an Allen Distinguished Investigator Award , and the Roger De Spoelberch Foundation Prize (to B.A.H.); Armenise-Harvard Foundation , AIRC , and CARITRO (to L.T.); and the European Research Council under the European Union’s Horizon 2020 research and innovation programme grant agreement no. 725780 LinPro (to S.H.). T.Z. and T.L. were supported by doctoral fellowships from the China Scholarship Council and A.H.H. by a doctoral DOC fellowship of the Austrian Academy of Sciences ( 24812 ). All animal work was conducted at the PHENO-ICMice facility. The Core is supported by 2 “Investissements d’avenir” (ANR-10- IAIHU-06 and ANR-11-INBS-0011-NeurATRIS) and the “Fondation pour la Recherche Médicale.” Light microscopy work was carried out at ICM’s imaging core facility, ICM.Quant, and analysis of scRNA-seq data was carried out at ICM’s bioinformatics core facility, iCONICS. We thank Paulina Ejsmont, Natalia Danda, and Nathalie De Geest for technical support. We are grateful to Dr. Shahragim TAJBAKHSH for providing R26Rstop-NICD-nGFP transgenic mice, Dr. Bart De Strooper for Psn1-deficient mice, Dr. Jean-Christophe Marine for Gt(ROSA)26SortdTom reporter mice, and Dr. Martinez Barbera for Sox2CreERT2 mice. We also give thanks to Dr. Mikio Hoshino for providing Atoh1 and Ptf1a antibodies. B.A.H. is an Einstein Visiting Fellow of the Berlin Institute of Health .","quality_controlled":"1","publisher":"Elsevier","oa":1,"day":"08","publication":"Cell Reports","isi":1,"has_accepted_license":"1","year":"2021","date_published":"2021-06-08T00:00:00Z","doi":"10.1016/j.celrep.2021.109208","date_created":"2020-09-21T12:00:48Z","article_number":"109208","project":[{"call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"},{"name":"Molecular Mechanisms of Radial Neuronal Migration","grant_number":"24812","_id":"2625A13E-B435-11E9-9278-68D0E5697425"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"chicago":"Zhang, Tingting, Tengyuan Liu, Natalia Mora, Justine Guegan, Mathilde Bertrand, Ximena Contreras, Andi H Hansen, et al. “Generation of Excitatory and Inhibitory Neurons from Common Progenitors via Notch Signaling in the Cerebellum.” Cell Reports. Elsevier, 2021. https://doi.org/10.1016/j.celrep.2021.109208.","ista":"Zhang T, Liu T, Mora N, Guegan J, Bertrand M, Contreras X, Hansen AH, Streicher C, Anderle M, Danda N, Tiberi L, Hippenmeyer S, Hassan BA. 2021. Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum. Cell Reports. 35(10), 109208.","mla":"Zhang, Tingting, et al. “Generation of Excitatory and Inhibitory Neurons from Common Progenitors via Notch Signaling in the Cerebellum.” Cell Reports, vol. 35, no. 10, 109208, Elsevier, 2021, doi:10.1016/j.celrep.2021.109208.","ieee":"T. Zhang et al., “Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum,” Cell Reports, vol. 35, no. 10. Elsevier, 2021.","short":"T. Zhang, T. Liu, N. Mora, J. Guegan, M. Bertrand, X. Contreras, A.H. Hansen, C. Streicher, M. Anderle, N. Danda, L. Tiberi, S. Hippenmeyer, B.A. Hassan, Cell Reports 35 (2021).","ama":"Zhang T, Liu T, Mora N, et al. Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum. Cell Reports. 2021;35(10). doi:10.1016/j.celrep.2021.109208","apa":"Zhang, T., Liu, T., Mora, N., Guegan, J., Bertrand, M., Contreras, X., … Hassan, B. A. (2021). Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum. Cell Reports. Elsevier. https://doi.org/10.1016/j.celrep.2021.109208"},"title":"Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum","author":[{"full_name":"Zhang, Tingting","last_name":"Zhang","first_name":"Tingting"},{"full_name":"Liu, Tengyuan","last_name":"Liu","first_name":"Tengyuan"},{"first_name":"Natalia","full_name":"Mora, Natalia","last_name":"Mora"},{"last_name":"Guegan","full_name":"Guegan, Justine","first_name":"Justine"},{"first_name":"Mathilde","last_name":"Bertrand","full_name":"Bertrand, Mathilde"},{"full_name":"Contreras, Ximena","last_name":"Contreras","id":"475990FE-F248-11E8-B48F-1D18A9856A87","first_name":"Ximena"},{"first_name":"Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87","last_name":"Hansen","full_name":"Hansen, Andi H"},{"id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","first_name":"Carmen","last_name":"Streicher","full_name":"Streicher, Carmen"},{"full_name":"Anderle, Marica","last_name":"Anderle","first_name":"Marica"},{"last_name":"Danda","full_name":"Danda, Natasha","first_name":"Natasha"},{"first_name":"Luca","last_name":"Tiberi","full_name":"Tiberi, Luca"},{"last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Bassem A.","full_name":"Hassan, Bassem A.","last_name":"Hassan"}],"external_id":{"pmid":["34107249 "],"isi":["000659894300001"]},"article_processing_charge":"No","oa_version":"Published Version","pmid":1,"abstract":[{"lang":"eng","text":"Brain neurons arise from relatively few progenitors generating an enormous diversity of neuronal types. Nonetheless, a cardinal feature of mammalian brain neurogenesis is thought to be that excitatory and inhibitory neurons derive from separate, spatially segregated progenitors. Whether bi-potential progenitors with an intrinsic capacity to generate both lineages exist and how such a fate decision may be regulated are unknown. Using cerebellar development as a model, we discover that individual progenitors can give rise to both inhibitory and excitatory lineages. Gradations of Notch activity determine the fates of the progenitors and their daughters. Daughters with the highest levels of Notch activity retain the progenitor fate, while intermediate levels of Notch activity generate inhibitory neurons, and daughters with very low levels of Notch signaling adopt the excitatory fate. Therefore, Notch-mediated binary cell fate choice is a mechanism for regulating the ratio of excitatory to inhibitory neurons from common progenitors."}],"month":"06","intvolume":" 35","scopus_import":"1","file":[{"file_size":8900385,"date_updated":"2021-06-15T14:01:35Z","creator":"cziletti","file_name":"2021_CellReports_Zhang.pdf","date_created":"2021-06-15T14:01:35Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","success":1,"file_id":"9554","checksum":"7def3d42ebc8f5675efb6f38819e3e2e"}],"language":[{"iso":"eng"}],"publication_identifier":{"eissn":[" 22111247"]},"publication_status":"published","volume":35,"issue":"10","related_material":{"link":[{"relation":"earlier_version","url":"https://doi.org/10.1101/2020.03.18.997205"}]},"license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","ec_funded":1,"_id":"8546","status":"public","article_type":"original","type":"journal_article","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"ddc":["570"],"date_updated":"2023-08-04T11:00:48Z","department":[{"_id":"SiHi"}],"file_date_updated":"2021-06-15T14:01:35Z"},{"oa":1,"quality_controlled":"1","publisher":"Elsevier","acknowledgement":"We thank Melissa Stouffer for critically reading the manuscript. This work was supported by IST Austria institutional funds; NÖ Forschung und Bildung n[f + b] life science call grant (C13-002) to S.H. and the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program (grant agreement 725780 LinPro) to S.H.","date_created":"2021-02-23T12:31:43Z","doi":"10.1016/j.neuint.2021.104986","date_published":"2021-05-01T00:00:00Z","publication":"Neurochemistry International","day":"01","year":"2021","has_accepted_license":"1","isi":1,"project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain","grant_number":"LS13-002","_id":"25D92700-B435-11E9-9278-68D0E5697425"}],"article_number":"104986","title":"Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond","article_processing_charge":"Yes (via OA deal)","external_id":{"isi":["000635575000005"],"pmid":["33600873"]},"author":[{"id":"48EA0138-F248-11E8-B48F-1D18A9856A87","first_name":"Florian","last_name":"Pauler","full_name":"Pauler, Florian"},{"first_name":"Quanah","full_name":"Hudson, Quanah","last_name":"Hudson"},{"id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","first_name":"Susanne","last_name":"Laukoter","full_name":"Laukoter, Susanne"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ista":"Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. 2021. Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry International. 145(5), 104986.","chicago":"Pauler, Florian, Quanah Hudson, Susanne Laukoter, and Simon Hippenmeyer. “Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell Level in Brain and Beyond.” Neurochemistry International. Elsevier, 2021. https://doi.org/10.1016/j.neuint.2021.104986.","ama":"Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry International. 2021;145(5). doi:10.1016/j.neuint.2021.104986","apa":"Pauler, F., Hudson, Q., Laukoter, S., & Hippenmeyer, S. (2021). Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry International. Elsevier. https://doi.org/10.1016/j.neuint.2021.104986","ieee":"F. Pauler, Q. Hudson, S. Laukoter, and S. Hippenmeyer, “Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond,” Neurochemistry International, vol. 145, no. 5. Elsevier, 2021.","short":"F. Pauler, Q. Hudson, S. Laukoter, S. Hippenmeyer, Neurochemistry International 145 (2021).","mla":"Pauler, Florian, et al. “Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell Level in Brain and Beyond.” Neurochemistry International, vol. 145, no. 5, 104986, Elsevier, 2021, doi:10.1016/j.neuint.2021.104986."},"intvolume":" 145","month":"05","scopus_import":"1","pmid":1,"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Genomic imprinting is an epigenetic mechanism that results in parental allele-specific expression of ~1% of all genes in mouse and human. Imprinted genes are key developmental regulators and play pivotal roles in many biological processes such as nutrient transfer from the mother to offspring and neuronal development. Imprinted genes are also involved in human disease, including neurodevelopmental disorders, and often occur in clusters that are regulated by a common imprint control region (ICR). In extra-embryonic tissues ICRs can act over large distances, with the largest surrounding Igf2r spanning over 10 million base-pairs. Besides classical imprinted expression that shows near exclusive maternal or paternal expression, widespread biased imprinted expression has been identified mainly in brain. In this review we discuss recent developments mapping cell type specific imprinted expression in extra-embryonic tissues and neocortex in the mouse. We highlight the advantages of using an inducible uniparental chromosome disomy (UPD) system to generate cells carrying either two maternal or two paternal copies of a specific chromosome to analyze the functional consequences of genomic imprinting. Mosaic Analysis with Double Markers (MADM) allows fluorescent labeling and concomitant induction of UPD sparsely in specific cell types, and thus to over-express or suppress all imprinted genes on that chromosome. To illustrate the utility of this technique, we explain how MADM-induced UPD revealed new insights about the function of the well-studied Cdkn1c imprinted gene, and how MADM-induced UPDs led to identification of highly cell type specific phenotypes related to perturbed imprinted expression in the mouse neocortex. Finally, we give an outlook on how MADM could be used to probe cell type specific imprinted expression in other tissues in mouse, particularly in extra-embryonic tissues."}],"ec_funded":1,"volume":145,"issue":"5","language":[{"iso":"eng"}],"file":[{"date_updated":"2021-08-11T12:30:38Z","file_size":7083499,"creator":"kschuh","date_created":"2021-08-11T12:30:38Z","file_name":"2021_NCI_Pauler.pdf","content_type":"application/pdf","access_level":"open_access","relation":"main_file","file_id":"9883","checksum":"c6d7a40089cd29e289f9b22e75768304","success":1}],"publication_status":"published","publication_identifier":{"issn":["0197-0186"]},"keyword":["Cell Biology","Cellular and Molecular Neuroscience"],"status":"public","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"type":"journal_article","article_type":"original","_id":"9188","file_date_updated":"2021-08-11T12:30:38Z","department":[{"_id":"SiHi"}],"ddc":["570"],"date_updated":"2023-08-07T13:48:26Z"},{"date_updated":"2023-08-10T13:53:23Z","ddc":["570"],"department":[{"_id":"SiHi"}],"file_date_updated":"2021-06-28T08:04:22Z","_id":"9601","type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","publication_identifier":{"eissn":["20411723"]},"publication_status":"published","file":[{"success":1,"checksum":"75dd89d09945185b2d14b2434a0bcb50","file_id":"9608","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2021_NatureCommunications_Santini.pdf","date_created":"2021-06-28T08:04:22Z","creator":"asandaue","file_size":2156554,"date_updated":"2021-06-28T08:04:22Z"}],"language":[{"iso":"eng"}],"volume":12,"issue":"1","abstract":[{"lang":"eng","text":"In mammalian genomes, differentially methylated regions (DMRs) and histone marks including trimethylation of histone 3 lysine 27 (H3K27me3) at imprinted genes are asymmetrically inherited to control parentally-biased gene expression. However, neither parent-of-origin-specific transcription nor imprints have been comprehensively mapped at the blastocyst stage of preimplantation development. Here, we address this by integrating transcriptomic and epigenomic approaches in mouse preimplantation embryos. We find that seventy-one genes exhibit previously unreported parent-of-origin-specific expression in blastocysts (nBiX: novel blastocyst-imprinted expressed). Uniparental expression of nBiX genes disappears soon after implantation. Micro-whole-genome bisulfite sequencing (µWGBS) of individual uniparental blastocysts detects 859 DMRs. We further find that 16% of nBiX genes are associated with a DMR, whereas most are associated with parentally-biased H3K27me3, suggesting a role for Polycomb-mediated imprinting in blastocysts. nBiX genes are clustered: five clusters contained at least one published imprinted gene, and five clusters exclusively contained nBiX genes. These data suggest that early development undergoes a complex program of stage-specific imprinting involving different tiers of regulation."}],"oa_version":"Published Version","scopus_import":"1","month":"07","intvolume":" 12","citation":{"ama":"Santini L, Halbritter F, Titz-Teixeira F, et al. Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3. Nature Communications. 2021;12(1). doi:10.1038/s41467-021-23510-4","apa":"Santini, L., Halbritter, F., Titz-Teixeira, F., Suzuki, T., Asami, M., Ma, X., … Leeb, M. (2021). Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-021-23510-4","short":"L. Santini, F. Halbritter, F. Titz-Teixeira, T. Suzuki, M. Asami, X. Ma, J. Ramesmayer, A. Lackner, N. Warr, F. Pauler, S. Hippenmeyer, E. Laue, M. Farlik, C. Bock, A. Beyer, A.C.F. Perry, M. Leeb, Nature Communications 12 (2021).","ieee":"L. Santini et al., “Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3,” Nature Communications, vol. 12, no. 1. Springer Nature, 2021.","mla":"Santini, Laura, et al. “Genomic Imprinting in Mouse Blastocysts Is Predominantly Associated with H3K27me3.” Nature Communications, vol. 12, no. 1, 3804, Springer Nature, 2021, doi:10.1038/s41467-021-23510-4.","ista":"Santini L, Halbritter F, Titz-Teixeira F, Suzuki T, Asami M, Ma X, Ramesmayer J, Lackner A, Warr N, Pauler F, Hippenmeyer S, Laue E, Farlik M, Bock C, Beyer A, Perry ACF, Leeb M. 2021. Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3. Nature Communications. 12(1), 3804.","chicago":"Santini, Laura, Florian Halbritter, Fabian Titz-Teixeira, Toru Suzuki, Maki Asami, Xiaoyan Ma, Julia Ramesmayer, et al. “Genomic Imprinting in Mouse Blastocysts Is Predominantly Associated with H3K27me3.” Nature Communications. Springer Nature, 2021. https://doi.org/10.1038/s41467-021-23510-4."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","author":[{"first_name":"Laura","last_name":"Santini","full_name":"Santini, Laura"},{"full_name":"Halbritter, Florian","last_name":"Halbritter","first_name":"Florian"},{"first_name":"Fabian","full_name":"Titz-Teixeira, Fabian","last_name":"Titz-Teixeira"},{"first_name":"Toru","full_name":"Suzuki, Toru","last_name":"Suzuki"},{"full_name":"Asami, Maki","last_name":"Asami","first_name":"Maki"},{"last_name":"Ma","full_name":"Ma, Xiaoyan","first_name":"Xiaoyan"},{"first_name":"Julia","last_name":"Ramesmayer","full_name":"Ramesmayer, Julia"},{"first_name":"Andreas","full_name":"Lackner, Andreas","last_name":"Lackner"},{"full_name":"Warr, Nick","last_name":"Warr","first_name":"Nick"},{"full_name":"Pauler, Florian","orcid":"0000-0002-7462-0048","last_name":"Pauler","first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"},{"first_name":"Ernest","full_name":"Laue, Ernest","last_name":"Laue"},{"first_name":"Matthias","full_name":"Farlik, Matthias","last_name":"Farlik"},{"last_name":"Bock","full_name":"Bock, Christoph","first_name":"Christoph"},{"last_name":"Beyer","full_name":"Beyer, Andreas","first_name":"Andreas"},{"first_name":"Anthony C.F.","last_name":"Perry","full_name":"Perry, Anthony C.F."},{"first_name":"Martin","full_name":"Leeb, Martin","last_name":"Leeb"}],"article_processing_charge":"No","external_id":{"isi":["000667248600005"]},"title":"Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3","article_number":"3804","isi":1,"has_accepted_license":"1","year":"2021","day":"12","publication":"Nature Communications","doi":"10.1038/s41467-021-23510-4","date_published":"2021-07-12T00:00:00Z","date_created":"2021-06-27T22:01:46Z","acknowledgement":"The authors thank Robert Feil and Anton Wutz for helpful discussions and comments, Samuel Collombet and Peter Fraser for sharing embryo TAD coordinates, and Andy Riddel at the Cambridge Stem Cell Institute and Thomas Sauer at the Max Perutz Laboratories FACS facility for flow-sorting. We thank the team of the Biomedical Sequencing Facility at the CeMM and the Vienna Biocenter Core Facilities (VBCF) for support with next-generation sequencing. We are grateful to animal care teams at the University of Bath and MRC Harwell. A.C.F.P. acknowledges support from the UK Medical Research Council (MR/N000080/1 and MR/N020294/1) and Biotechnology and Biological Sciences Research Council (BB/P009506/1). L.S. is part of the FWF doctoral programme SMICH and supported by an Austrian Academy of Sciences DOC Fellowship. M.L. is funded by a Vienna Research Group for Young Investigators grant (VRG14-006) by the Vienna Science and Technology Fund (WWTF) and by the Austrian Science Fund FWF (I3786 and P31334).","quality_controlled":"1","publisher":"Springer Nature","oa":1},{"acknowledgement":"We thank the Bioimaging, Life Science, and Pre-Clinical Facilities at IST Austria; M.P. Postiglione, C. Simbriger, K. Valoskova, C. Schwayer, T. Hussain, M. Pieber, and V. Wimmer for initial experiments, technical support, and/or assistance; R. Shigemoto for sharing iv (Dnah11 mutant) mice; and M. Sixt and all members of the Hippenmeyer lab for discussion. This work was supported by National Institutes of Health grants ( R01-NS050580 to L.L. and F32MH096361 to L.A.S.). L.L. is an investigator of HHMI. N.A. received support from FWF Firnberg-Programm ( T 1031 ). A.H.H. is a recipient of a DOC Fellowship (24812) of the Austrian Academy of Sciences . This work also received support from IST Austria institutional funds , FWF SFB F78 to S.H., the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme ( FP7/2007-2013 ) under REA grant agreement no 618444 to S.H., and the European Research Council (ERC) under the European Union’s Horizon 2020 Research and Innovation Programme (grant agreement no. 725780 LinPro ) to S.H.","publisher":"Cell Press","quality_controlled":"1","oa":1,"day":"22","publication":"Cell Reports","isi":1,"has_accepted_license":"1","year":"2021","date_published":"2021-06-22T00:00:00Z","doi":"10.1016/j.celrep.2021.109274","date_created":"2021-06-27T22:01:48Z","article_number":"109274","project":[{"name":"Molecular Mechanisms of Radial Neuronal Migration","grant_number":"24812","_id":"2625A13E-B435-11E9-9278-68D0E5697425"},{"call_identifier":"FP7","_id":"25D61E48-B435-11E9-9278-68D0E5697425","name":"Molecular Mechanisms of Cerebral Cortex Development","grant_number":"618444"},{"call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"apa":"Contreras, X., Amberg, N., Davaatseren, A., Hansen, A. H., Sonntag, J., Andersen, L., … Hippenmeyer, S. (2021). A genome-wide library of MADM mice for single-cell genetic mosaic analysis. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2021.109274","ama":"Contreras X, Amberg N, Davaatseren A, et al. A genome-wide library of MADM mice for single-cell genetic mosaic analysis. Cell Reports. 2021;35(12). doi:10.1016/j.celrep.2021.109274","short":"X. Contreras, N. Amberg, A. Davaatseren, A.H. Hansen, J. Sonntag, L. Andersen, T. Bernthaler, C. Streicher, A.-M. Heger, R.L. Johnson, L.A. Schwarz, L. Luo, T. Rülicke, S. Hippenmeyer, Cell Reports 35 (2021).","ieee":"X. Contreras et al., “A genome-wide library of MADM mice for single-cell genetic mosaic analysis,” Cell Reports, vol. 35, no. 12. Cell Press, 2021.","mla":"Contreras, Ximena, et al. “A Genome-Wide Library of MADM Mice for Single-Cell Genetic Mosaic Analysis.” Cell Reports, vol. 35, no. 12, 109274, Cell Press, 2021, doi:10.1016/j.celrep.2021.109274.","ista":"Contreras X, Amberg N, Davaatseren A, Hansen AH, Sonntag J, Andersen L, Bernthaler T, Streicher C, Heger A-M, Johnson RL, Schwarz LA, Luo L, Rülicke T, Hippenmeyer S. 2021. A genome-wide library of MADM mice for single-cell genetic mosaic analysis. Cell Reports. 35(12), 109274.","chicago":"Contreras, Ximena, Nicole Amberg, Amarbayasgalan Davaatseren, Andi H Hansen, Johanna Sonntag, Lill Andersen, Tina Bernthaler, et al. “A Genome-Wide Library of MADM Mice for Single-Cell Genetic Mosaic Analysis.” Cell Reports. Cell Press, 2021. https://doi.org/10.1016/j.celrep.2021.109274."},"title":"A genome-wide library of MADM mice for single-cell genetic mosaic analysis","author":[{"id":"475990FE-F248-11E8-B48F-1D18A9856A87","first_name":"Ximena","full_name":"Contreras, Ximena","last_name":"Contreras"},{"first_name":"Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-3183-8207","full_name":"Amberg, Nicole","last_name":"Amberg"},{"id":"70ADC922-B424-11E9-99E3-BA18E6697425","first_name":"Amarbayasgalan","last_name":"Davaatseren","full_name":"Davaatseren, Amarbayasgalan"},{"id":"38853E16-F248-11E8-B48F-1D18A9856A87","first_name":"Andi H","last_name":"Hansen","full_name":"Hansen, Andi H"},{"id":"32FE7D7C-F248-11E8-B48F-1D18A9856A87","first_name":"Johanna","full_name":"Sonntag, Johanna","last_name":"Sonntag"},{"last_name":"Andersen","full_name":"Andersen, Lill","first_name":"Lill"},{"last_name":"Bernthaler","full_name":"Bernthaler, Tina","first_name":"Tina"},{"id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","first_name":"Carmen","full_name":"Streicher, Carmen","last_name":"Streicher"},{"id":"4B76FFD2-F248-11E8-B48F-1D18A9856A87","first_name":"Anna-Magdalena","last_name":"Heger","full_name":"Heger, Anna-Magdalena"},{"full_name":"Johnson, Randy L.","last_name":"Johnson","first_name":"Randy L."},{"first_name":"Lindsay A.","full_name":"Schwarz, Lindsay A.","last_name":"Schwarz"},{"first_name":"Liqun","last_name":"Luo","full_name":"Luo, Liqun"},{"first_name":"Thomas","last_name":"Rülicke","full_name":"Rülicke, Thomas"},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"external_id":{"isi":["000664463600016"]},"article_processing_charge":"No","oa_version":"Published Version","acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"},{"_id":"PreCl"}],"abstract":[{"text":"Mosaic analysis with double markers (MADM) offers one approach to visualize and concomitantly manipulate genetically defined cells in mice with single-cell resolution. MADM applications include the analysis of lineage, single-cell morphology and physiology, genomic imprinting phenotypes, and dissection of cell-autonomous gene functions in vivo in health and disease. Yet, MADM can only be applied to <25% of all mouse genes on select chromosomes to date. To overcome this limitation, we generate transgenic mice with knocked-in MADM cassettes near the centromeres of all 19 autosomes and validate their use across organs. With this resource, >96% of the entire mouse genome can now be subjected to single-cell genetic mosaic analysis. Beyond a proof of principle, we apply our MADM library to systematically trace sister chromatid segregation in distinct mitotic cell lineages. We find striking chromosome-specific biases in segregation patterns, reflecting a putative mechanism for the asymmetric segregation of genetic determinants in somatic stem cell division.","lang":"eng"}],"month":"06","intvolume":" 35","scopus_import":"1","file":[{"creator":"asandaue","date_updated":"2021-06-28T14:06:24Z","file_size":7653149,"date_created":"2021-06-28T14:06:24Z","file_name":"2021_CellReports_Contreras.pdf","access_level":"open_access","relation":"main_file","content_type":"application/pdf","file_id":"9613","checksum":"d49520fdcbbb5c2f883bddb67cee5d77","success":1}],"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["22111247"]},"publication_status":"published","related_material":{"link":[{"relation":"press_release","url":"https://ist.ac.at/en/news/boost-for-mouse-genetic-analysis/","description":"News on IST Homepage"}]},"volume":35,"issue":"12","ec_funded":1,"_id":"9603","status":"public","type":"journal_article","article_type":"original","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"ddc":["570"],"date_updated":"2023-08-10T13:55:00Z","department":[{"_id":"SiHi"},{"_id":"LoSw"},{"_id":"PreCl"}],"file_date_updated":"2021-06-28T14:06:24Z"},{"abstract":[{"text":"Endometriosis is a common gynecological disorder characterized by ectopic growth of endometrium outside the uterus and is associated with chronic pain and infertility. We investigated the role of the long intergenic noncoding RNA 01133 (LINC01133) in endometriosis, an lncRNA that has been implicated in several types of cancer. We found that LINC01133 is upregulated in ectopic endometriotic lesions. As expression appeared higher in the epithelial endometrial layer, we performed a siRNA knockdown of LINC01133 in an endometriosis epithelial cell line. Phenotypic assays indicated that LINC01133 may promote proliferation and suppress cellular migration, and affect the cytoskeleton and morphology of the cells. Gene ontology analysis of differentially expressed genes indicated that cell proliferation and migration pathways were affected in line with the observed phenotype. We validated upregulation of p21 and downregulation of Cyclin A at the protein level, which together with the quantification of the DNA content using fluorescence-activated cell sorting (FACS) analysis indicated that the observed effects on cellular proliferation may be due to changes in cell cycle. Further, we found testis-specific protein kinase 1 (TESK1) kinase upregulation corresponding with phosphorylation and inactivation of actin severing protein Cofilin, which could explain changes in the cytoskeleton and cellular migration. These results indicate that endometriosis is associated with LINC01133 upregulation, which may affect pathogenesis via the cellular proliferation and migration pathways.","lang":"eng"}],"oa_version":"Published Version","scopus_import":"1","month":"08","intvolume":" 22","publication_identifier":{"issn":["16616596"],"eissn":["14220067"]},"publication_status":"published","file":[{"success":1,"file_id":"9922","checksum":"be7f0042607ca60549cb27513c19c6af","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2021_InternationalJournalOfMolecularSciences_Yotova.pdf","date_created":"2021-08-16T09:29:17Z","creator":"asandaue","file_size":2646018,"date_updated":"2021-08-16T09:29:17Z"}],"language":[{"iso":"eng"}],"volume":22,"issue":"16","_id":"9906","type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","date_updated":"2023-08-11T10:34:13Z","ddc":["570"],"file_date_updated":"2021-08-16T09:29:17Z","department":[{"_id":"SiHi"}],"acknowledgement":"Open access funding provided by Medical University of Vienna. The authors would like to thank all the participants and health professionals involved in the present study. We want to thank our technical assistants Barbara Widmar and Matthias Witzmann-Stern for their diligent work and constant assistance. We would like to thank Simon Hippenmeyer for access to\r\nbioinformatic infrastructure and resources.","publisher":"MDPI","quality_controlled":"1","oa":1,"isi":1,"has_accepted_license":"1","year":"2021","day":"04","publication":"International Journal of Molecular Sciences","doi":"10.3390/ijms22168385","date_published":"2021-08-04T00:00:00Z","date_created":"2021-08-15T22:01:27Z","article_number":"8385","citation":{"chicago":"Yotova, Iveta, Quanah J. Hudson, Florian Pauler, Katharina Proestling, Isabella Haslinger, Lorenz Kuessel, Alexandra Perricos, Heinrich Husslein, and René Wenzl. “LINC01133 Inhibits Invasion and Promotes Proliferation in an Endometriosis Epithelial Cell Line.” International Journal of Molecular Sciences. MDPI, 2021. https://doi.org/10.3390/ijms22168385.","ista":"Yotova I, Hudson QJ, Pauler F, Proestling K, Haslinger I, Kuessel L, Perricos A, Husslein H, Wenzl R. 2021. LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line. International Journal of Molecular Sciences. 22(16), 8385.","mla":"Yotova, Iveta, et al. “LINC01133 Inhibits Invasion and Promotes Proliferation in an Endometriosis Epithelial Cell Line.” International Journal of Molecular Sciences, vol. 22, no. 16, 8385, MDPI, 2021, doi:10.3390/ijms22168385.","ieee":"I. Yotova et al., “LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line,” International Journal of Molecular Sciences, vol. 22, no. 16. MDPI, 2021.","short":"I. Yotova, Q.J. Hudson, F. Pauler, K. Proestling, I. Haslinger, L. Kuessel, A. Perricos, H. Husslein, R. Wenzl, International Journal of Molecular Sciences 22 (2021).","apa":"Yotova, I., Hudson, Q. J., Pauler, F., Proestling, K., Haslinger, I., Kuessel, L., … Wenzl, R. (2021). LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line. International Journal of Molecular Sciences. MDPI. https://doi.org/10.3390/ijms22168385","ama":"Yotova I, Hudson QJ, Pauler F, et al. LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line. International Journal of Molecular Sciences. 2021;22(16). doi:10.3390/ijms22168385"},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","author":[{"last_name":"Yotova","full_name":"Yotova, Iveta","first_name":"Iveta"},{"full_name":"Hudson, Quanah J.","last_name":"Hudson","first_name":"Quanah J."},{"last_name":"Pauler","orcid":"0000-0002-7462-0048","full_name":"Pauler, Florian","first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Katharina","last_name":"Proestling","full_name":"Proestling, Katharina"},{"first_name":"Isabella","last_name":"Haslinger","full_name":"Haslinger, Isabella"},{"last_name":"Kuessel","full_name":"Kuessel, Lorenz","first_name":"Lorenz"},{"last_name":"Perricos","full_name":"Perricos, Alexandra","first_name":"Alexandra"},{"first_name":"Heinrich","last_name":"Husslein","full_name":"Husslein, Heinrich"},{"first_name":"René","full_name":"Wenzl, René","last_name":"Wenzl"}],"external_id":{"isi":["000689147400001"]},"article_processing_charge":"Yes","title":"LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line"},{"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"chicago":"Hanganu-Opatz, Ileana L., Simon J. B. Butt, Simon Hippenmeyer, Natalia V. De Marco García, Jessica A. Cardin, Bradley Voytek, and Alysson R. Muotri. “The Logic of Developing Neocortical Circuits in Health and Disease.” The Journal of Neuroscience. Society for Neuroscience, 2021. https://doi.org/10.1523/jneurosci.1655-20.2020.","ista":"Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, De Marco García NV, Cardin JA, Voytek B, Muotri AR. 2021. The logic of developing neocortical circuits in health and disease. The Journal of Neuroscience. 41(5), 813–822.","mla":"Hanganu-Opatz, Ileana L., et al. “The Logic of Developing Neocortical Circuits in Health and Disease.” The Journal of Neuroscience, vol. 41, no. 5, Society for Neuroscience, 2021, pp. 813–22, doi:10.1523/jneurosci.1655-20.2020.","short":"I.L. Hanganu-Opatz, S.J.B. Butt, S. Hippenmeyer, N.V. De Marco García, J.A. Cardin, B. Voytek, A.R. Muotri, The Journal of Neuroscience 41 (2021) 813–822.","ieee":"I. L. Hanganu-Opatz et al., “The logic of developing neocortical circuits in health and disease,” The Journal of Neuroscience, vol. 41, no. 5. Society for Neuroscience, pp. 813–822, 2021.","apa":"Hanganu-Opatz, I. L., Butt, S. J. B., Hippenmeyer, S., De Marco García, N. V., Cardin, J. A., Voytek, B., & Muotri, A. R. (2021). The logic of developing neocortical circuits in health and disease. The Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/jneurosci.1655-20.2020","ama":"Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, et al. The logic of developing neocortical circuits in health and disease. The Journal of Neuroscience. 2021;41(5):813-822. doi:10.1523/jneurosci.1655-20.2020"},"title":"The logic of developing neocortical circuits in health and disease","article_processing_charge":"No","external_id":{"isi":["000616763400002"],"pmid":["33431633"]},"author":[{"full_name":"Hanganu-Opatz, Ileana L.","last_name":"Hanganu-Opatz","first_name":"Ileana L."},{"last_name":"Butt","full_name":"Butt, Simon J. B.","first_name":"Simon J. B."},{"orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"},{"full_name":"De Marco García, Natalia V.","last_name":"De Marco García","first_name":"Natalia V."},{"full_name":"Cardin, Jessica A.","last_name":"Cardin","first_name":"Jessica A."},{"full_name":"Voytek, Bradley","last_name":"Voytek","first_name":"Bradley"},{"full_name":"Muotri, Alysson R.","last_name":"Muotri","first_name":"Alysson R."}],"project":[{"_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"},{"_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E","grant_number":"F07805","name":"Molecular Mechanisms of Neural Stem Cell Lineage Progression"}],"publication":"The Journal of Neuroscience","day":"03","year":"2021","isi":1,"has_accepted_license":"1","date_created":"2021-02-03T12:23:51Z","date_published":"2021-02-03T00:00:00Z","doi":"10.1523/jneurosci.1655-20.2020","page":"813-822","acknowledgement":"Work in the I.L.H.-O. laboratory was supported by European Research Council Grant ERC-2015-CoG 681577 and German Research Foundation Ha 4466/10-1, Ha4466/11-1, Ha4466/12-1, SPP 1665, and SFB 936B5. Work in the S.J.B.B. laboratory was supported by Biotechnology and Biological Sciences Research Council BB/P003796/1, Medical Research Council MR/K004387/1 and MR/T033320/1, Wellcome Trust 215199/Z/19/Z and 102386/Z/13/Z, and John Fell Fund. Work in the S.H. laboratory was supported by European Research Council Grants ERC-2016-CoG 725780 LinPro and FWF SFB F78. This work was supported by National Institutes of Health Grant NIMH 1R01MH110553 to N.V.D.M.G. Work in the J.A.C. laboratory was supported by the Ludwig Family Foundation, Simons Foundation SFARI Research Award, and National Institutes of Health/National Institute of Mental Health R01 MH102365 and R01MH113852. The B.V. laboratory was supported by Whitehall Foundation 2017-12-73, National Science Foundation 1736028, National Institutes of Health, National Institute of General Medical Sciences R01GM134363-01, and Halıcıoğlu Data Science Institute Fellowship. This work was supported by the University of California San Diego School of Medicine.","oa":1,"quality_controlled":"1","publisher":"Society for Neuroscience","ddc":["570"],"date_updated":"2023-09-05T14:03:17Z","file_date_updated":"2022-05-27T06:59:55Z","department":[{"_id":"SiHi"}],"_id":"9073","keyword":["General Neuroscience"],"status":"public","type":"journal_article","article_type":"original","language":[{"iso":"eng"}],"file":[{"success":1,"checksum":"578fd7ed1a0aef74bce61bea2d987b33","file_id":"11414","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2021_JourNeuroscience_Hanganu.pdf","date_created":"2022-05-27T06:59:55Z","creator":"dernst","file_size":1031150,"date_updated":"2022-05-27T06:59:55Z"}],"publication_status":"published","publication_identifier":{"eissn":["1529-2401"],"issn":["0270-6474"]},"ec_funded":1,"issue":"5","volume":41,"pmid":1,"oa_version":"Published Version","abstract":[{"lang":"eng","text":"The sensory and cognitive abilities of the mammalian neocortex are underpinned by intricate columnar and laminar circuits formed from an array of diverse neuronal populations. One approach to determining how interactions between these circuit components give rise to complex behavior is to investigate the rules by which cortical circuits are formed and acquire functionality during development. This review summarizes recent research on the development of the neocortex, from genetic determination in neural stem cells through to the dynamic role that specific neuronal populations play in the earliest circuits of neocortex, and how they contribute to emergent function and cognition. While many of these endeavors take advantage of model systems, consideration will also be given to advances in our understanding of activity in nascent human circuits. Such cross-species perspective is imperative when investigating the mechanisms underlying the dysfunction of early neocortical circuits in neurodevelopmental disorders, so that one can identify targets amenable to therapeutic intervention."}],"intvolume":" 41","month":"02","scopus_import":"1"},{"_id":"9793","status":"public","type":"journal_article","article_type":"original","date_updated":"2023-09-27T07:46:09Z","department":[{"_id":"SiHi"}],"pmid":1,"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Astrocytes extensively infiltrate the neuropil to regulate critical aspects of synaptic development and function. This process is regulated by transcellular interactions between astrocytes and neurons via cell adhesion molecules. How astrocytes coordinate developmental processes among one another to parse out the synaptic neuropil and form non-overlapping territories is unknown. Here we identify a molecular mechanism regulating astrocyte-astrocyte interactions during development to coordinate astrocyte morphogenesis and gap junction coupling. We show that hepaCAM, a disease-linked, astrocyte-enriched cell adhesion molecule, regulates astrocyte competition for territory and morphological complexity in the developing mouse cortex. Furthermore, conditional deletion of Hepacam from developing astrocytes significantly impairs gap junction coupling between astrocytes and disrupts the balance between synaptic excitation and inhibition. Mutations in HEPACAM cause megalencephalic leukoencephalopathy with subcortical cysts in humans. Therefore, our findings suggest that disruption of astrocyte self-organization mechanisms could be an underlying cause of neural pathology."}],"month":"08","intvolume":" 109","scopus_import":"1","main_file_link":[{"url":"https://doi.org/10.1016/j.neuron.2021.05.025","open_access":"1"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0896-6273"],"eissn":["1097-4199"]},"publication_status":"published","volume":109,"issue":"15","ec_funded":1,"project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"apa":"Baldwin, K. T., Tan, C. X., Strader, S. T., Jiang, C., Savage, J. T., Elorza-Vidal, X., … Eroglu, C. (2021). HepaCAM controls astrocyte self-organization and coupling. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2021.05.025","ama":"Baldwin KT, Tan CX, Strader ST, et al. HepaCAM controls astrocyte self-organization and coupling. Neuron. 2021;109(15):2427-2442.e10. doi:10.1016/j.neuron.2021.05.025","short":"K.T. Baldwin, C.X. Tan, S.T. Strader, C. Jiang, J.T. Savage, X. Elorza-Vidal, X. Contreras, T. Rülicke, S. Hippenmeyer, R. Estévez, R.-R. Ji, C. Eroglu, Neuron 109 (2021) 2427–2442.e10.","ieee":"K. T. Baldwin et al., “HepaCAM controls astrocyte self-organization and coupling,” Neuron, vol. 109, no. 15. Elsevier, p. 2427–2442.e10, 2021.","mla":"Baldwin, Katherine T., et al. “HepaCAM Controls Astrocyte Self-Organization and Coupling.” Neuron, vol. 109, no. 15, Elsevier, 2021, p. 2427–2442.e10, doi:10.1016/j.neuron.2021.05.025.","ista":"Baldwin KT, Tan CX, Strader ST, Jiang C, Savage JT, Elorza-Vidal X, Contreras X, Rülicke T, Hippenmeyer S, Estévez R, Ji R-R, Eroglu C. 2021. HepaCAM controls astrocyte self-organization and coupling. Neuron. 109(15), 2427–2442.e10.","chicago":"Baldwin, Katherine T., Christabel X. Tan, Samuel T. Strader, Changyu Jiang, Justin T. Savage, Xabier Elorza-Vidal, Ximena Contreras, et al. “HepaCAM Controls Astrocyte Self-Organization and Coupling.” Neuron. Elsevier, 2021. https://doi.org/10.1016/j.neuron.2021.05.025."},"title":"HepaCAM controls astrocyte self-organization and coupling","author":[{"first_name":"Katherine T.","full_name":"Baldwin, Katherine T.","last_name":"Baldwin"},{"first_name":"Christabel X.","full_name":"Tan, Christabel X.","last_name":"Tan"},{"first_name":"Samuel T.","full_name":"Strader, Samuel T.","last_name":"Strader"},{"last_name":"Jiang","full_name":"Jiang, Changyu","first_name":"Changyu"},{"last_name":"Savage","full_name":"Savage, Justin T.","first_name":"Justin T."},{"full_name":"Elorza-Vidal, Xabier","last_name":"Elorza-Vidal","first_name":"Xabier"},{"first_name":"Ximena","id":"475990FE-F248-11E8-B48F-1D18A9856A87","last_name":"Contreras","full_name":"Contreras, Ximena"},{"last_name":"Rülicke","full_name":"Rülicke, Thomas","first_name":"Thomas"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer"},{"last_name":"Estévez","full_name":"Estévez, Raúl","first_name":"Raúl"},{"first_name":"Ru-Rong","full_name":"Ji, Ru-Rong","last_name":"Ji"},{"first_name":"Cagla","last_name":"Eroglu","full_name":"Eroglu, Cagla"}],"article_processing_charge":"No","external_id":{"pmid":["34171291"],"isi":["000692851900010"]},"acknowledgement":"This work was supported by the National Institutes of Health (R01 DA047258 and R01 NS102237 to C.E., F32 NS100392 to K.T.B.) and the Holland-Trice Brain Research Award (to C.E.). K.T.B. was supported by postdoctoral fellowships from the Foerster-Bernstein Family and The Hartwell Foundation. The Hippenmeyer lab was supported by the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovations program (725780 LinPro) to S.H. R.E. was supported by Ministerio de Ciencia y Tecnología (RTI2018-093493-B-I00). We thank the Duke Light Microscopy Core Facility, the Duke Transgenic Mouse Facility, Dr. U. Schulte for assistance with proteomic experiments, and Dr. D. Silver for critical review of the manuscript. Cartoon elements of figure panels were created using BioRender.com.","publisher":"Elsevier","quality_controlled":"1","oa":1,"day":"04","publication":"Neuron","isi":1,"year":"2021","date_published":"2021-08-04T00:00:00Z","doi":"10.1016/j.neuron.2021.05.025","date_created":"2021-08-06T09:08:25Z","page":"2427-2442.e10"},{"year":"2021","has_accepted_license":"1","isi":1,"publication":"Molecular Therapy - Methods and Clinical Development","day":"10","page":"210-224","date_created":"2022-01-23T23:01:28Z","doi":"10.1016/j.omtm.2021.09.006","date_published":"2021-12-10T00:00:00Z","acknowledgement":"This project has received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 715571). The research was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Bioimaging Facility, the Life Science Facility, and the Pre-Clinical Facility, namely Sonja Haslinger and Michael Schunn for their animal colony management and support. We would also like to thank Chakrabarty Lab for sharing the plasmids for AAV2/6 production. Finally, we would like to thank the Siegert team members for discussion about the manuscript.","oa":1,"publisher":"Elsevier","quality_controlled":"1","citation":{"ieee":"M. E. Maes, G. M. Wögenstein, G. Colombo, R. Casado Polanco, and S. Siegert, “Optimizing AAV2/6 microglial targeting identified enhanced efficiency in the photoreceptor degenerative environment,” Molecular Therapy - Methods and Clinical Development, vol. 23. Elsevier, pp. 210–224, 2021.","short":"M.E. Maes, G.M. Wögenstein, G. Colombo, R. Casado Polanco, S. Siegert, Molecular Therapy - Methods and Clinical Development 23 (2021) 210–224.","ama":"Maes ME, Wögenstein GM, Colombo G, Casado Polanco R, Siegert S. Optimizing AAV2/6 microglial targeting identified enhanced efficiency in the photoreceptor degenerative environment. Molecular Therapy - Methods and Clinical Development. 2021;23:210-224. doi:10.1016/j.omtm.2021.09.006","apa":"Maes, M. E., Wögenstein, G. M., Colombo, G., Casado Polanco, R., & Siegert, S. (2021). Optimizing AAV2/6 microglial targeting identified enhanced efficiency in the photoreceptor degenerative environment. Molecular Therapy - Methods and Clinical Development. Elsevier. https://doi.org/10.1016/j.omtm.2021.09.006","mla":"Maes, Margaret E., et al. “Optimizing AAV2/6 Microglial Targeting Identified Enhanced Efficiency in the Photoreceptor Degenerative Environment.” Molecular Therapy - Methods and Clinical Development, vol. 23, Elsevier, 2021, pp. 210–24, doi:10.1016/j.omtm.2021.09.006.","ista":"Maes ME, Wögenstein GM, Colombo G, Casado Polanco R, Siegert S. 2021. Optimizing AAV2/6 microglial targeting identified enhanced efficiency in the photoreceptor degenerative environment. Molecular Therapy - Methods and Clinical Development. 23, 210–224.","chicago":"Maes, Margaret E, Gabriele M. Wögenstein, Gloria Colombo, Raquel Casado Polanco, and Sandra Siegert. “Optimizing AAV2/6 Microglial Targeting Identified Enhanced Efficiency in the Photoreceptor Degenerative Environment.” Molecular Therapy - Methods and Clinical Development. Elsevier, 2021. https://doi.org/10.1016/j.omtm.2021.09.006."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","external_id":{"isi":["000748748500019"]},"article_processing_charge":"Yes","author":[{"first_name":"Margaret E","id":"3838F452-F248-11E8-B48F-1D18A9856A87","full_name":"Maes, Margaret E","orcid":"0000-0001-9642-1085","last_name":"Maes"},{"last_name":"Wögenstein","full_name":"Wögenstein, Gabriele M.","first_name":"Gabriele M."},{"full_name":"Colombo, Gloria","orcid":"0000-0001-9434-8902","last_name":"Colombo","id":"3483CF6C-F248-11E8-B48F-1D18A9856A87","first_name":"Gloria"},{"id":"15240fc1-dbcd-11ea-9d1d-ac5a786425fd","first_name":"Raquel","full_name":"Casado Polanco, Raquel","orcid":"0000-0001-8293-4568","last_name":"Casado Polanco"},{"full_name":"Siegert, Sandra","orcid":"0000-0001-8635-0877","last_name":"Siegert","id":"36ACD32E-F248-11E8-B48F-1D18A9856A87","first_name":"Sandra"}],"title":"Optimizing AAV2/6 microglial targeting identified enhanced efficiency in the photoreceptor degenerative environment","project":[{"_id":"25D4A630-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"Microglia action towards neuronal circuit formation and function in health and disease","grant_number":"715571"}],"publication_status":"published","publication_identifier":{"eissn":["2329-0501"]},"language":[{"iso":"eng"}],"file":[{"file_name":"2021_MolTherMethodsClinDev_Maes.pdf","date_created":"2022-01-24T07:43:09Z","creator":"cchlebak","file_size":4794147,"date_updated":"2022-01-24T07:43:09Z","success":1,"file_id":"10657","checksum":"77dc540e8011c5475031bdf6ccef20a6","relation":"main_file","access_level":"open_access","content_type":"application/pdf"}],"ec_funded":1,"volume":23,"acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"},{"_id":"PreCl"}],"abstract":[{"text":"Adeno-associated viruses (AAVs) are widely used to deliver genetic material in vivo to distinct cell types such as neurons or glial cells, allowing for targeted manipulation. Transduction of microglia is mostly excluded from this strategy, likely due to the cells’ heterogeneous state upon environmental changes, which makes AAV design challenging. Here, we established the retina as a model system for microglial AAV validation and optimization. First, we show that AAV2/6 transduced microglia in both synaptic layers, where layer preference corresponds to the intravitreal or subretinal delivery method. Surprisingly, we observed significantly enhanced microglial transduction during photoreceptor degeneration. Thus, we modified the AAV6 capsid to reduce heparin binding by introducing four point mutations (K531E, R576Q, K493S, and K459S), resulting in increased microglial transduction in the outer plexiform layer. Finally, to improve microglial-specific transduction, we validated a Cre-dependent transgene delivery cassette for use in combination with the Cx3cr1CreERT2 mouse line. Together, our results provide a foundation for future studies optimizing AAV-mediated microglia transduction and highlight that environmental conditions influence microglial transduction efficiency.\r\n","lang":"eng"}],"oa_version":"Published Version","scopus_import":"1","intvolume":" 23","month":"12","date_updated":"2023-11-16T13:12:03Z","ddc":["570"],"file_date_updated":"2022-01-24T07:43:09Z","department":[{"_id":"SaSi"},{"_id":"SiHi"}],"_id":"10655","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"original","type":"journal_article","status":"public"},{"abstract":[{"text":"Mosaic analysis with double markers (MADM) technology enables the generation of genetic mosaic tissue in mice. MADM enables concomitant fluorescent cell labeling and introduction of a mutation of a gene of interest with single-cell resolution. This protocol highlights major steps for the generation of genetic mosaic tissue and the isolation and processing of respective tissues for downstream histological analysis. For complete details on the use and execution of this protocol, please refer to Contreras et al. (2021).","lang":"eng"}],"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"oa_version":"Published Version","scopus_import":"1","month":"11","intvolume":" 2","publication_identifier":{"eissn":["2666-1667"]},"publication_status":"published","file":[{"creator":"cchlebak","file_size":7309464,"date_updated":"2021-11-22T08:23:58Z","file_name":"2021_STARProtocols_Amberg.pdf","date_created":"2021-11-22T08:23:58Z","relation":"main_file","access_level":"open_access","content_type":"application/pdf","success":1,"file_id":"10329","checksum":"9e3f6d06bf583e7a8b6a9e9a60500a28"}],"language":[{"iso":"eng"}],"issue":"4","volume":2,"ec_funded":1,"_id":"10321","type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","date_updated":"2023-11-16T13:08:03Z","ddc":["573"],"department":[{"_id":"SiHi"}],"file_date_updated":"2021-11-22T08:23:58Z","acknowledgement":"This research was supported by the Scientific Service Units (SSU) at IST Austria through resources provided by the Bioimaging (BIF) and Preclinical Facilities (PCF). We particularly thank Mohammad Goudarzi for assistance with photography of mouse perfusion and dissection. N.A. received support from FWF Firnberg-Programm (T 1031). This work was also supported by IST Austria institutional funds; FWF SFB F78 to S.H.; and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 725780 LinPro) to S.H.","publisher":"Cell Press","quality_controlled":"1","oa":1,"has_accepted_license":"1","year":"2021","day":"10","publication":"STAR Protocols","doi":"10.1016/j.xpro.2021.100939","date_published":"2021-11-10T00:00:00Z","date_created":"2021-11-21T23:01:28Z","article_number":"100939","project":[{"call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"},{"call_identifier":"FWF","_id":"268F8446-B435-11E9-9278-68D0E5697425","name":"Role of Eed in neural stem cell lineage progression","grant_number":"T0101031"},{"grant_number":"F07805","name":"Molecular Mechanisms of Neural Stem Cell Lineage Progression","_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E"}],"citation":{"chicago":"Amberg, Nicole, and Simon Hippenmeyer. “Genetic Mosaic Dissection of Candidate Genes in Mice Using Mosaic Analysis with Double Markers.” STAR Protocols. Cell Press, 2021. https://doi.org/10.1016/j.xpro.2021.100939.","ista":"Amberg N, Hippenmeyer S. 2021. Genetic mosaic dissection of candidate genes in mice using mosaic analysis with double markers. STAR Protocols. 2(4), 100939.","mla":"Amberg, Nicole, and Simon Hippenmeyer. “Genetic Mosaic Dissection of Candidate Genes in Mice Using Mosaic Analysis with Double Markers.” STAR Protocols, vol. 2, no. 4, 100939, Cell Press, 2021, doi:10.1016/j.xpro.2021.100939.","ama":"Amberg N, Hippenmeyer S. Genetic mosaic dissection of candidate genes in mice using mosaic analysis with double markers. STAR Protocols. 2021;2(4). doi:10.1016/j.xpro.2021.100939","apa":"Amberg, N., & Hippenmeyer, S. (2021). Genetic mosaic dissection of candidate genes in mice using mosaic analysis with double markers. STAR Protocols. Cell Press. https://doi.org/10.1016/j.xpro.2021.100939","short":"N. Amberg, S. Hippenmeyer, STAR Protocols 2 (2021).","ieee":"N. Amberg and S. Hippenmeyer, “Genetic mosaic dissection of candidate genes in mice using mosaic analysis with double markers,” STAR Protocols, vol. 2, no. 4. Cell Press, 2021."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","author":[{"last_name":"Amberg","orcid":"0000-0002-3183-8207","full_name":"Amberg, Nicole","first_name":"Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"}],"article_processing_charge":"Yes","title":"Genetic mosaic dissection of candidate genes in mice using mosaic analysis with double markers"},{"intvolume":" 109","month":"02","main_file_link":[{"url":"https://doi.org/10.1101/2020.06.14.151258","open_access":"1"}],"scopus_import":"1","oa_version":"Preprint","abstract":[{"text":"The synaptotrophic hypothesis posits that synapse formation stabilizes dendritic branches, yet this hypothesis has not been causally tested in vivo in the mammalian brain. Presynaptic ligand cerebellin-1 (Cbln1) and postsynaptic receptor GluD2 mediate synaptogenesis between granule cells and Purkinje cells in the molecular layer of the cerebellar cortex. Here we show that sparse but not global knockout of GluD2 causes under-elaboration of Purkinje cell dendrites in the deep molecular layer and overelaboration in the superficial molecular layer. Developmental, overexpression, structure-function, and genetic epistasis analyses indicate that dendrite morphogenesis defects result from competitive synaptogenesis in a Cbln1/GluD2-dependent manner. A generative model of dendritic growth based on competitive synaptogenesis largely recapitulates GluD2 sparse and global knockout phenotypes. Our results support the synaptotrophic hypothesis at initial stages of dendrite development, suggest a second mode in which cumulative synapse formation inhibits further dendrite growth, and highlight the importance of competition in dendrite morphogenesis.","lang":"eng"}],"ec_funded":1,"volume":109,"issue":"4","language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"eissn":["1097-4199"]},"status":"public","article_type":"original","type":"journal_article","_id":"8544","department":[{"_id":"SiHi"}],"date_updated":"2024-03-06T12:12:48Z","oa":1,"quality_controlled":"1","publisher":"Elsevier","acknowledgement":"We thank M. Mishina for GluD2fl frozen embryos, T.C. Südhof and J.I. Morgan for Cbln1fl mice, L. Anderson for help in generating the MADM alleles, W. Joo for a previously unpublished construct, M. Yuzaki, K. Shen, J. Ding, and members of the Luo lab, including J.M. Kebschull, H. Li, J. Li, T. Li, C.M. McLaughlin, D. Pederick, J. Ren, D.C. Wang and C. Xu for discussions and critiques of the manuscript, and M. Yuzaki for supporting Y.H.T. during the final phase of this project. Y.H.T. was supported by a JSPS fellowship; S.A.S. was supported by a Stanford Graduate Fellowship and an NSF Predoctoral Fellowship; L.J. is supported by a Stanford Graduate Fellowship and an NSF Predoctoral Fellowship; M.J.W. is supported by a Burroughs Wellcome Fund CASI Award. This work was supported by an NIH grant (R01-NS050538) to L.L.; the European Research Council (ERC) under the European Union's Horizon 2020 research and innovations programme (No. 725780 LinPro) to S.H.; and Simons and James S. McDonnell Foundations and an NSF CAREER award to S.G.; L.L. is an HHMI investigator.","date_created":"2020-09-21T11:59:47Z","doi":"10.1016/j.neuron.2020.11.028","date_published":"2021-02-17T00:00:00Z","page":"P629-644.E8","publication":"Neuron","day":"17","year":"2021","project":[{"_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"}],"title":"GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells","article_processing_charge":"No","author":[{"first_name":"Yukari H.","last_name":"Takeo","full_name":"Takeo, Yukari H."},{"first_name":"S. Andrew","full_name":"Shuster, S. Andrew","last_name":"Shuster"},{"first_name":"Linnie","full_name":"Jiang, Linnie","last_name":"Jiang"},{"last_name":"Hu","full_name":"Hu, Miley","first_name":"Miley"},{"last_name":"Luginbuhl","full_name":"Luginbuhl, David J.","first_name":"David J."},{"last_name":"Rülicke","full_name":"Rülicke, Thomas","first_name":"Thomas"},{"id":"475990FE-F248-11E8-B48F-1D18A9856A87","first_name":"Ximena","full_name":"Contreras, Ximena","last_name":"Contreras"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061"},{"full_name":"Wagner, Mark J.","last_name":"Wagner","first_name":"Mark J."},{"full_name":"Ganguli, Surya","last_name":"Ganguli","first_name":"Surya"},{"first_name":"Liqun","last_name":"Luo","full_name":"Luo, Liqun"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Takeo, Yukari H., et al. “GluD2- and Cbln1-Mediated Competitive Synaptogenesis Shapes the Dendritic Arbors of Cerebellar Purkinje Cells.” Neuron, vol. 109, no. 4, Elsevier, 2021, p. P629–644.E8, doi:10.1016/j.neuron.2020.11.028.","short":"Y.H. Takeo, S.A. Shuster, L. Jiang, M. Hu, D.J. Luginbuhl, T. Rülicke, X. Contreras, S. Hippenmeyer, M.J. Wagner, S. Ganguli, L. Luo, Neuron 109 (2021) P629–644.E8.","ieee":"Y. H. Takeo et al., “GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells,” Neuron, vol. 109, no. 4. Elsevier, p. P629–644.E8, 2021.","apa":"Takeo, Y. H., Shuster, S. A., Jiang, L., Hu, M., Luginbuhl, D. J., Rülicke, T., … Luo, L. (2021). GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2020.11.028","ama":"Takeo YH, Shuster SA, Jiang L, et al. GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. Neuron. 2021;109(4):P629-644.E8. doi:10.1016/j.neuron.2020.11.028","chicago":"Takeo, Yukari H., S. Andrew Shuster, Linnie Jiang, Miley Hu, David J. Luginbuhl, Thomas Rülicke, Ximena Contreras, et al. “GluD2- and Cbln1-Mediated Competitive Synaptogenesis Shapes the Dendritic Arbors of Cerebellar Purkinje Cells.” Neuron. Elsevier, 2021. https://doi.org/10.1016/j.neuron.2020.11.028.","ista":"Takeo YH, Shuster SA, Jiang L, Hu M, Luginbuhl DJ, Rülicke T, Contreras X, Hippenmeyer S, Wagner MJ, Ganguli S, Luo L. 2021. GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. Neuron. 109(4), P629–644.E8."}},{"title":"Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration","author":[{"id":"38853E16-F248-11E8-B48F-1D18A9856A87","first_name":"Andi H","full_name":"Hansen, Andi H","last_name":"Hansen"}],"article_processing_charge":"No","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"ista":"Hansen AH. 2021. Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration. Institute of Science and Technology Austria.","chicago":"Hansen, Andi H. “Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects in Radial Projection Neuron Migration.” Institute of Science and Technology Austria, 2021. https://doi.org/10.15479/at:ista:9962.","short":"A.H. Hansen, Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects in Radial Projection Neuron Migration, Institute of Science and Technology Austria, 2021.","ieee":"A. H. Hansen, “Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration,” Institute of Science and Technology Austria, 2021.","ama":"Hansen AH. Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration. 2021. doi:10.15479/at:ista:9962","apa":"Hansen, A. H. (2021). Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration. Institute of Science and Technology Austria. https://doi.org/10.15479/at:ista:9962","mla":"Hansen, Andi H. Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects in Radial Projection Neuron Migration. Institute of Science and Technology Austria, 2021, doi:10.15479/at:ista:9962."},"project":[{"grant_number":"24812","name":"Molecular Mechanisms of Radial Neuronal Migration","_id":"2625A13E-B435-11E9-9278-68D0E5697425"}],"doi":"10.15479/at:ista:9962","date_published":"2021-09-02T00:00:00Z","date_created":"2021-08-29T12:36:50Z","page":"182","day":"02","has_accepted_license":"1","year":"2021","publisher":"Institute of Science and Technology Austria","oa":1,"file_date_updated":"2022-09-03T22:30:04Z","department":[{"_id":"GradSch"},{"_id":"SiHi"}],"ddc":["570"],"supervisor":[{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon"}],"date_updated":"2023-09-22T09:58:30Z","status":"public","keyword":["Neuronal migration","Non-cell-autonomous","Cell-autonomous","Neurodevelopmental disease"],"type":"dissertation","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"9962","related_material":{"record":[{"relation":"part_of_dissertation","status":"public","id":"8569"},{"status":"public","id":"960","relation":"part_of_dissertation"}]},"file":[{"creator":"ahansen","file_size":10629190,"date_updated":"2022-09-03T22:30:04Z","file_name":"Thesis_Hansen.docx","date_created":"2021-08-30T09:17:39Z","relation":"source_file","access_level":"closed","embargo_to":"open_access","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","file_id":"9971","checksum":"66b56f5b988b233dc66a4f4b4fb2cdfe"},{"checksum":"204fa40321a1c6289b68c473634c4bf3","file_id":"9972","embargo":"2022-09-02","access_level":"open_access","relation":"main_file","content_type":"application/pdf","date_created":"2021-08-30T09:29:44Z","file_name":"Thesis_Hansen_PDFA-1a.pdf","creator":"ahansen","date_updated":"2022-09-03T22:30:04Z","file_size":13457469}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2663-337X"]},"degree_awarded":"PhD","publication_status":"published","month":"09","alternative_title":["ISTA Thesis"],"oa_version":"Published Version","abstract":[{"lang":"eng","text":"The brain is one of the largest and most complex organs and it is composed of billions of neurons that communicate together enabling e.g. consciousness. The cerebral cortex is the largest site of neural integration in the central nervous system. Concerted radial migration of newly born cortical projection neurons, from their birthplace to their final position, is a key step in the assembly of the cerebral cortex. The cellular and molecular mechanisms regulating radial neuronal migration in vivo are however still unclear. Recent evidence suggests that distinct signaling cues act cell-autonomously but differentially at certain steps during the overall migration process. Moreover, functional analysis of genetic mosaics (mutant neurons present in wild-type/heterozygote environment) using the MADM (Mosaic Analysis with Double Markers) analyses in comparison to global knockout also indicate a significant degree of non-cell-autonomous and/or community effects in the control of cortical neuron migration. The interactions of cell-intrinsic (cell-autonomous) and cell-extrinsic (non-cell-autonomous) components are largely unknown. In part of this thesis work we established a MADM-based experimental strategy for the quantitative analysis of cell-autonomous gene function versus non-cell-autonomous and/or community effects. The direct comparison of mutant neurons from the genetic mosaic (cell-autonomous) to mutant neurons in the conditional and/or global knockout (cell-autonomous + non-cell-autonomous) allows to quantitatively analyze non-cell-autonomous effects. Such analysis enable the high-resolution analysis of projection neuron migration dynamics in distinct environments with concomitant isolation of genomic and proteomic profiles. Using these experimental paradigms and in combination with computational modeling we show and characterize the nature of non-cell-autonomous effects to coordinate radial neuron migration. Furthermore, this thesis discusses recent developments in neurodevelopment with focus on neuronal polarization and non-cell-autonomous mechanisms in neuronal migration."}]},{"ec_funded":1,"volume":5,"publication_status":"published","publication_identifier":{"issn":["2504-284X"]},"language":[{"iso":"eng"}],"file":[{"creator":"dernst","date_updated":"2020-07-14T12:48:03Z","file_size":1402146,"date_created":"2020-05-11T11:34:08Z","file_name":"2020_FrontiersEduc_Beattie.pdf","access_level":"open_access","relation":"main_file","content_type":"application/pdf","checksum":"a24ec24e38d843341ae620ec76c53688","file_id":"7818"}],"intvolume":" 5","month":"05","acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"},{"_id":"PreCl"},{"_id":"EM-Fac"}],"abstract":[{"text":"Scientific research is to date largely restricted to wealthy laboratories in developed nations due to the necessity of complex and expensive equipment. This inequality limits the capacity of science to be used as a diplomatic channel. Maker movements use open-source technologies including additive manufacturing (3D printing) and laser cutting, together with low-cost computers for developing novel products. This movement is setting the groundwork for a revolution, allowing scientific equipment to be sourced at a fraction of the cost and has the potential to increase the availability of equipment for scientists around the world. Science education is increasingly recognized as another channel for science diplomacy. In this perspective, we introduce the idea that the Maker movement and open-source technologies have the potential to revolutionize science, technology, engineering and mathematics (STEM) education worldwide. We present an open-source STEM didactic tool called SCOPES (Sparking Curiosity through Open-source Platforms in Education and Science). SCOPES is self-contained, independent of local resources, and cost-effective. SCOPES can be adapted to communicate complex subjects from genetics to neurobiology, perform real-world biological experiments and explore digitized scientific samples. We envision such platforms will enhance science diplomacy by providing a means for scientists to share their findings with classrooms and for educators to incorporate didactic concepts into STEM lessons. By providing students the opportunity to design, perform, and share scientific experiments, students also experience firsthand the benefits of a multinational scientific community. We provide instructions on how to build and use SCOPES on our webpage: http://scopeseducation.org.","lang":"eng"}],"oa_version":"Published Version","file_date_updated":"2020-07-14T12:48:03Z","department":[{"_id":"SiHi"}],"date_updated":"2021-01-12T08:15:42Z","ddc":["570"],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","status":"public","_id":"7814","date_created":"2020-05-11T08:18:48Z","date_published":"2020-05-08T00:00:00Z","doi":"10.3389/feduc.2020.00048","year":"2020","has_accepted_license":"1","publication":"Frontiers in Education","day":"08","oa":1,"publisher":"Frontiers Media","quality_controlled":"1","article_processing_charge":"No","author":[{"first_name":"Robert J","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8483-8753","full_name":"Beattie, Robert J","last_name":"Beattie"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"},{"first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","last_name":"Pauler","full_name":"Pauler, Florian"}],"title":"SCOPES: Sparking curiosity through Open-Source platforms in education and science","citation":{"chicago":"Beattie, Robert J, Simon Hippenmeyer, and Florian Pauler. “SCOPES: Sparking Curiosity through Open-Source Platforms in Education and Science.” Frontiers in Education. Frontiers Media, 2020. https://doi.org/10.3389/feduc.2020.00048.","ista":"Beattie RJ, Hippenmeyer S, Pauler F. 2020. SCOPES: Sparking curiosity through Open-Source platforms in education and science. Frontiers in Education. 5, 48.","mla":"Beattie, Robert J., et al. “SCOPES: Sparking Curiosity through Open-Source Platforms in Education and Science.” Frontiers in Education, vol. 5, 48, Frontiers Media, 2020, doi:10.3389/feduc.2020.00048.","ieee":"R. J. Beattie, S. Hippenmeyer, and F. Pauler, “SCOPES: Sparking curiosity through Open-Source platforms in education and science,” Frontiers in Education, vol. 5. Frontiers Media, 2020.","short":"R.J. Beattie, S. Hippenmeyer, F. Pauler, Frontiers in Education 5 (2020).","apa":"Beattie, R. J., Hippenmeyer, S., & Pauler, F. (2020). SCOPES: Sparking curiosity through Open-Source platforms in education and science. Frontiers in Education. Frontiers Media. https://doi.org/10.3389/feduc.2020.00048","ama":"Beattie RJ, Hippenmeyer S, Pauler F. SCOPES: Sparking curiosity through Open-Source platforms in education and science. Frontiers in Education. 2020;5. doi:10.3389/feduc.2020.00048"},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","project":[{"_id":"264E56E2-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex","grant_number":"M02416"},{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}],"article_number":"48"},{"citation":{"ista":"Gao X, Li J-L, Chen X, Ci B, Chen F, Lu N, Shen B, Zheng L, Jia J-M, Yi Y, Zhang S, Shi Y-C, Shi K, Propson NE, Huang Y, Poinsatte K, Zhang Z, Yue Y, Bosco DB, Lu Y, Yang S, Adams RH, Lindner V, Huang F, Wu L-J, Zheng H, Han F, Hippenmeyer S, Stowe AM, Peng B, Margeta M, Wang X, Liu Q, Körbelin J, Trepel M, Lu H, Zhou BO, Zhao H, Su W, Bachoo RM, Ge W. Reduction of neuronal activity mediated by blood-vessel regression in the brain. bioRxiv, 10.1101/2020.09.15.262782.","chicago":"Gao, Xiaofei, Jun-Liszt Li, Xingjun Chen, Bo Ci, Fei Chen, Nannan Lu, Bo Shen, et al. “Reduction of Neuronal Activity Mediated by Blood-Vessel Regression in the Brain.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2020.09.15.262782.","ieee":"X. Gao et al., “Reduction of neuronal activity mediated by blood-vessel regression in the brain,” bioRxiv. Cold Spring Harbor Laboratory.","short":"X. Gao, J.-L. Li, X. Chen, B. Ci, F. Chen, N. Lu, B. Shen, L. Zheng, J.-M. Jia, Y. Yi, S. Zhang, Y.-C. Shi, K. Shi, N.E. Propson, Y. Huang, K. Poinsatte, Z. Zhang, Y. Yue, D.B. Bosco, Y. Lu, S. Yang, R.H. Adams, V. Lindner, F. Huang, L.-J. Wu, H. Zheng, F. Han, S. Hippenmeyer, A.M. Stowe, B. Peng, M. Margeta, X. Wang, Q. Liu, J. Körbelin, M. Trepel, H. Lu, B.O. Zhou, H. Zhao, W. Su, R.M. Bachoo, W. Ge, BioRxiv (n.d.).","ama":"Gao X, Li J-L, Chen X, et al. Reduction of neuronal activity mediated by blood-vessel regression in the brain. bioRxiv. doi:10.1101/2020.09.15.262782","apa":"Gao, X., Li, J.-L., Chen, X., Ci, B., Chen, F., Lu, N., … Ge, W. (n.d.). Reduction of neuronal activity mediated by blood-vessel regression in the brain. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2020.09.15.262782","mla":"Gao, Xiaofei, et al. “Reduction of Neuronal Activity Mediated by Blood-Vessel Regression in the Brain.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2020.09.15.262782."},"date_updated":"2021-01-12T08:20:19Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","author":[{"last_name":"Gao","full_name":"Gao, Xiaofei","first_name":"Xiaofei"},{"last_name":"Li","full_name":"Li, Jun-Liszt","first_name":"Jun-Liszt"},{"last_name":"Chen","full_name":"Chen, Xingjun","first_name":"Xingjun"},{"last_name":"Ci","full_name":"Ci, Bo","first_name":"Bo"},{"first_name":"Fei","last_name":"Chen","full_name":"Chen, Fei"},{"last_name":"Lu","full_name":"Lu, Nannan","first_name":"Nannan"},{"first_name":"Bo","last_name":"Shen","full_name":"Shen, Bo"},{"first_name":"Lijun","full_name":"Zheng, Lijun","last_name":"Zheng"},{"first_name":"Jie-Min","last_name":"Jia","full_name":"Jia, Jie-Min"},{"last_name":"Yi","full_name":"Yi, Yating","first_name":"Yating"},{"first_name":"Shiwen","full_name":"Zhang, Shiwen","last_name":"Zhang"},{"full_name":"Shi, Ying-Chao","last_name":"Shi","first_name":"Ying-Chao"},{"full_name":"Shi, Kaibin","last_name":"Shi","first_name":"Kaibin"},{"first_name":"Nicholas E","last_name":"Propson","full_name":"Propson, Nicholas E"},{"full_name":"Huang, Yubin","last_name":"Huang","first_name":"Yubin"},{"first_name":"Katherine","full_name":"Poinsatte, Katherine","last_name":"Poinsatte"},{"last_name":"Zhang","full_name":"Zhang, Zhaohuan","first_name":"Zhaohuan"},{"last_name":"Yue","full_name":"Yue, Yuanlei","first_name":"Yuanlei"},{"first_name":"Dale B","full_name":"Bosco, Dale B","last_name":"Bosco"},{"full_name":"Lu, Ying-mei","last_name":"Lu","first_name":"Ying-mei"},{"last_name":"Yang","full_name":"Yang, Shi-bing","first_name":"Shi-bing"},{"last_name":"Adams","full_name":"Adams, Ralf H.","first_name":"Ralf H."},{"first_name":"Volkhard","last_name":"Lindner","full_name":"Lindner, Volkhard"},{"first_name":"Fen","last_name":"Huang","full_name":"Huang, Fen"},{"full_name":"Wu, Long-Jun","last_name":"Wu","first_name":"Long-Jun"},{"first_name":"Hui","last_name":"Zheng","full_name":"Zheng, Hui"},{"first_name":"Feng","full_name":"Han, Feng","last_name":"Han"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061"},{"first_name":"Ann M.","last_name":"Stowe","full_name":"Stowe, Ann M."},{"last_name":"Peng","full_name":"Peng, Bo","first_name":"Bo"},{"full_name":"Margeta, Marta","last_name":"Margeta","first_name":"Marta"},{"last_name":"Wang","full_name":"Wang, Xiaoqun","first_name":"Xiaoqun"},{"first_name":"Qiang","last_name":"Liu","full_name":"Liu, Qiang"},{"full_name":"Körbelin, Jakob","last_name":"Körbelin","first_name":"Jakob"},{"last_name":"Trepel","full_name":"Trepel, Martin","first_name":"Martin"},{"first_name":"Hui","last_name":"Lu","full_name":"Lu, Hui"},{"full_name":"Zhou, Bo O.","last_name":"Zhou","first_name":"Bo O."},{"first_name":"Hu","last_name":"Zhao","full_name":"Zhao, Hu"},{"last_name":"Su","full_name":"Su, Wenzhi","first_name":"Wenzhi"},{"first_name":"Robert M.","last_name":"Bachoo","full_name":"Bachoo, Robert M."},{"first_name":"Woo-ping","last_name":"Ge","full_name":"Ge, Woo-ping"}],"title":"Reduction of neuronal activity mediated by blood-vessel regression in the brain","department":[{"_id":"SiHi"}],"_id":"8616","type":"preprint","status":"public","project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425"}],"year":"2020","publication_status":"submitted","publication":"bioRxiv","language":[{"iso":"eng"}],"day":"15","date_created":"2020-10-06T08:58:59Z","ec_funded":1,"doi":"10.1101/2020.09.15.262782","date_published":"2020-09-15T00:00:00Z","abstract":[{"lang":"eng","text":"The brain vasculature supplies neurons with glucose and oxygen, but little is known about how vascular plasticity contributes to brain function. Using longitudinal in vivo imaging, we reported that a substantial proportion of blood vessels in the adult brain sporadically occluded and regressed. Their regression proceeded through sequential stages of blood-flow occlusion, endothelial cell collapse, relocation or loss of pericytes, and retraction of glial endfeet. Regressing vessels were found to be widespread in mouse, monkey and human brains. Both brief occlusions of the middle cerebral artery and lipopolysaccharide-mediated inflammation induced an increase of vessel regression. Blockage of leukocyte adhesion to endothelial cells alleviated LPS-induced vessel regression. We further revealed that blood vessel regression caused a reduction of neuronal activity due to a dysfunction in mitochondrial metabolism and glutamate production. Our results elucidate the mechanism of vessel regression and its role in neuronal function in the adult brain."}],"acknowledgement":"The project was initiated in the Jan lab at UCSF. We thank Lily Jan and Yuh-Nung Jan’s generous support. We thank Liqun Luo’s lab for providing MADM-7 mice and Rolf A Brekken for VEGF-antibodies. Drs. Yuanquan Song (UPenn), Zhaozhu Hu (JHU), Ji Hu (ShanghaiTech), Yang Xiang (U. Mass), Hao Wang (Zhejiang U.) and Ruikang Wang (U. Washington) for critical input, colleagues at Children’s Research Institute, Departments of Neuroscience, Neurology and Neurotherapeutics, Pediatrics from UT Southwestern, and colleagues from the Jan lab for discussion. Dr. Bridget Samuels, Sean Morrison (UT Southwestern), and Nannan Lu (Zhejiang U.) for critical reading. We acknowledge the assistance of the CIBR Imaging core. We also thank UT Southwestern Live Cell Imaging Facility, a Shared Resource of the Harold C. Simmons Cancer Center, supported in part by an NCI Cancer Center Support Grant, P30 CA142543K. This work is supported by CIBR funds and the American Heart Association AWRP Summer 2016 Innovative Research Grant (17IRG33410377) to W-P.G.; National Natural Science Foundation of China (No.81370031) to Z.Z.;National Key Research and Development Program of China (2016YFE0125400)to F.H.;National Natural Science Foundations of China (No. 81473202) to Y.L.; National Natural Science Foundation of China (No.31600839) and Shenzhen Science and Technology Research Program (JCYJ20170818163320865) to B.P.; National Natural Science Foundation of China (No. 31800864) and Westlake University start-up funds to J-M. J. NIH R01NS088627 to W.L.J.; NIH: R01 AG020670 and RF1AG054111 to H.Z.; R01 NS088555 to A.M.S., and European Research Council No.725780 to S.H.;W-P.G. was a recipient of Bugher-American Heart Association Dan Adams Thinking Outside the Box Award.","oa_version":"Preprint","main_file_link":[{"url":"https://doi.org/10.1101/2020.09.15.262782","open_access":"1"}],"oa":1,"publisher":"Cold Spring Harbor Laboratory","month":"09"},{"article_number":"100215","project":[{"name":"Role of Eed in neural stem cell lineage progression","grant_number":"T0101031","_id":"268F8446-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"grant_number":"F07805","name":"Molecular Mechanisms of Neural Stem Cell Lineage Progression","_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E"},{"name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain","grant_number":"LS13-002","_id":"25D92700-B435-11E9-9278-68D0E5697425"},{"name":"Molecular Mechanisms of Cerebral Cortex Development","grant_number":"618444","_id":"25D61E48-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425"}],"citation":{"mla":"Laukoter, Susanne, et al. “Generation and Isolation of Single Cells from Mouse Brain with Mosaic Analysis with Double Markers-Induced Uniparental Chromosome Disomy.” STAR Protocols, vol. 1, no. 3, 100215, Elsevier, 2020, doi:10.1016/j.xpro.2020.100215.","apa":"Laukoter, S., Amberg, N., Pauler, F., & Hippenmeyer, S. (2020). Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy. STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2020.100215","ama":"Laukoter S, Amberg N, Pauler F, Hippenmeyer S. Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy. STAR Protocols. 2020;1(3). doi:10.1016/j.xpro.2020.100215","short":"S. Laukoter, N. Amberg, F. Pauler, S. Hippenmeyer, STAR Protocols 1 (2020).","ieee":"S. Laukoter, N. Amberg, F. Pauler, and S. Hippenmeyer, “Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy,” STAR Protocols, vol. 1, no. 3. Elsevier, 2020.","chicago":"Laukoter, Susanne, Nicole Amberg, Florian Pauler, and Simon Hippenmeyer. “Generation and Isolation of Single Cells from Mouse Brain with Mosaic Analysis with Double Markers-Induced Uniparental Chromosome Disomy.” STAR Protocols. Elsevier, 2020. https://doi.org/10.1016/j.xpro.2020.100215.","ista":"Laukoter S, Amberg N, Pauler F, Hippenmeyer S. 2020. Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy. STAR Protocols. 1(3), 100215."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","external_id":{"pmid":["33377108"]},"author":[{"first_name":"Susanne","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","last_name":"Laukoter","full_name":"Laukoter, Susanne"},{"last_name":"Amberg","full_name":"Amberg, Nicole","orcid":"0000-0002-3183-8207","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","first_name":"Nicole"},{"last_name":"Pauler","full_name":"Pauler, Florian","first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"}],"title":"Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy","acknowledgement":"This research was supported by the Scientific Service Units (SSU) at IST Austria through resources provided by the Bioimaging (BIF) and Preclinical Facilities (PCF). N.A received support from the FWF Firnberg-Programm (T 1031). This work was also supported by IST Austria institutional funds; FWF SFB F78 to S.H.; NÖ Forschung und Bildung n[f+b] life science call grant (C13-002) to S.H.; the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement no. 618444 to S.H.; and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 725780 LinPro) to S.H.","oa":1,"publisher":"Elsevier","quality_controlled":"1","year":"2020","has_accepted_license":"1","publication":"STAR Protocols","day":"18","date_created":"2020-12-30T10:17:07Z","date_published":"2020-12-18T00:00:00Z","doi":"10.1016/j.xpro.2020.100215","_id":"8978","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"article_type":"original","type":"journal_article","status":"public","date_updated":"2021-01-12T08:21:36Z","ddc":["570"],"department":[{"_id":"SiHi"}],"file_date_updated":"2021-01-07T15:57:27Z","abstract":[{"lang":"eng","text":"Mosaic analysis with double markers (MADM) technology enables concomitant fluorescent cell labeling and induction of uniparental chromosome disomy (UPD) with single-cell resolution. In UPD, imprinted genes are either overexpressed 2-fold or are not expressed. Here, the MADM platform is utilized to probe imprinting phenotypes at the transcriptional level. This protocol highlights major steps for the generation and isolation of projection neurons and astrocytes with MADM-induced UPD from mouse cerebral cortex for downstream single-cell and low-input sample RNA-sequencing experiments.\r\n\r\nFor complete details on the use and execution of this protocol, please refer to Laukoter et al. (2020b)."}],"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"oa_version":"Published Version","pmid":1,"intvolume":" 1","month":"12","publication_status":"published","publication_identifier":{"issn":["2666-1667"]},"language":[{"iso":"eng"}],"file":[{"content_type":"application/pdf","relation":"main_file","access_level":"open_access","success":1,"file_id":"8996","checksum":"f1e9a433e9cb0f41f7b6df6b76db1f6e","file_size":4031449,"date_updated":"2021-01-07T15:57:27Z","creator":"dernst","file_name":"2020_STARProtocols_Laukoter.pdf","date_created":"2021-01-07T15:57:27Z"}],"ec_funded":1,"volume":1,"issue":"3"},{"doi":"10.1038/s41467-019-14077-2","date_published":"2020-01-10T00:00:00Z","date_created":"2020-01-11T10:42:48Z","day":"10","publication":"Nature Communications","has_accepted_license":"1","isi":1,"year":"2020","quality_controlled":"1","publisher":"Springer Nature","oa":1,"title":"Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development","author":[{"first_name":"Susanne","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7903-3010","full_name":"Laukoter, Susanne","last_name":"Laukoter"},{"first_name":"Robert J","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","full_name":"Beattie, Robert J","orcid":"0000-0002-8483-8753","last_name":"Beattie"},{"id":"48EA0138-F248-11E8-B48F-1D18A9856A87","first_name":"Florian","last_name":"Pauler","orcid":"0000-0002-7462-0048","full_name":"Pauler, Florian"},{"id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","first_name":"Nicole","last_name":"Amberg","full_name":"Amberg, Nicole","orcid":"0000-0002-3183-8207"},{"full_name":"Nakayama, Keiichi I.","last_name":"Nakayama","first_name":"Keiichi I."},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"article_processing_charge":"No","external_id":{"isi":["000551459000005"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"mla":"Laukoter, Susanne, et al. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously Promotes Cell Survival in Cerebral Cortex Development.” Nature Communications, vol. 11, 195, Springer Nature, 2020, doi:10.1038/s41467-019-14077-2.","ieee":"S. Laukoter, R. J. Beattie, F. Pauler, N. Amberg, K. I. Nakayama, and S. Hippenmeyer, “Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development,” Nature Communications, vol. 11. Springer Nature, 2020.","short":"S. Laukoter, R.J. Beattie, F. Pauler, N. Amberg, K.I. Nakayama, S. Hippenmeyer, Nature Communications 11 (2020).","apa":"Laukoter, S., Beattie, R. J., Pauler, F., Amberg, N., Nakayama, K. I., & Hippenmeyer, S. (2020). Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-019-14077-2","ama":"Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. Nature Communications. 2020;11. doi:10.1038/s41467-019-14077-2","chicago":"Laukoter, Susanne, Robert J Beattie, Florian Pauler, Nicole Amberg, Keiichi I. Nakayama, and Simon Hippenmeyer. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously Promotes Cell Survival in Cerebral Cortex Development.” Nature Communications. Springer Nature, 2020. https://doi.org/10.1038/s41467-019-14077-2.","ista":"Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. 2020. Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. Nature Communications. 11, 195."},"project":[{"call_identifier":"FWF","_id":"268F8446-B435-11E9-9278-68D0E5697425","grant_number":"T0101031","name":"Role of Eed in neural stem cell lineage progression"},{"name":"Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex","grant_number":"M02416","_id":"264E56E2-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain","grant_number":"LS13-002","_id":"25D92700-B435-11E9-9278-68D0E5697425"}],"article_number":"195","volume":11,"related_material":{"link":[{"description":"News on IST Homepage","relation":"press_release","url":"https://ist.ac.at/en/news/new-function-for-potential-tumour-suppressor-in-brain-development/"}]},"ec_funded":1,"file":[{"file_size":8063333,"date_updated":"2020-07-14T12:47:54Z","creator":"dernst","file_name":"2020_NatureComm_Laukoter.pdf","date_created":"2020-01-13T07:42:31Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","checksum":"ebf1ed522f4e0be8d94c939c1806a709","file_id":"7261"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2041-1723"]},"publication_status":"published","month":"01","intvolume":" 11","scopus_import":"1","oa_version":"Published Version","acknowledged_ssus":[{"_id":"PreCl"}],"abstract":[{"lang":"eng","text":"The cyclin-dependent kinase inhibitor p57KIP2 is encoded by the imprinted Cdkn1c locus, exhibits maternal expression, and is essential for cerebral cortex development. How Cdkn1c regulates corticogenesis is however not clear. To this end we employ Mosaic Analysis with Double Markers (MADM) technology to genetically dissect Cdkn1c gene function in corticogenesis at single cell resolution. We find that the previously described growth-inhibitory Cdkn1c function is a non-cell-autonomous one, acting on the whole organism. In contrast we reveal a growth-promoting cell-autonomous Cdkn1c function which at the mechanistic level mediates radial glial progenitor cell and nascent projection neuron survival. Strikingly, the growth-promoting function of Cdkn1c is highly dosage sensitive but not subject to genomic imprinting. Collectively, our results suggest that the Cdkn1c locus regulates cortical development through distinct cell-autonomous and non-cell-autonomous mechanisms. More generally, our study highlights the importance to probe the relative contributions of cell intrinsic gene function and tissue-wide mechanisms to the overall phenotype."}],"department":[{"_id":"SiHi"}],"file_date_updated":"2020-07-14T12:47:54Z","ddc":["570"],"date_updated":"2023-08-17T14:23:41Z","status":"public","type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"7253"},{"title":"LIS1 determines cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility","external_id":{"pmid":["32159512"],"isi":["000522835800001"]},"article_processing_charge":"No","author":[{"first_name":"Hyang Mi","last_name":"Moon","full_name":"Moon, Hyang Mi"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer"},{"full_name":"Luo, Liqun","last_name":"Luo","first_name":"Liqun"},{"first_name":"Anthony","last_name":"Wynshaw-Boris","full_name":"Wynshaw-Boris, Anthony"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"mla":"Moon, Hyang Mi, et al. “LIS1 Determines Cleavage Plane Positioning by Regulating Actomyosin-Mediated Cell Membrane Contractility.” ELife, vol. 9, 51512, eLife Sciences Publications, 2020, doi:10.7554/elife.51512.","apa":"Moon, H. M., Hippenmeyer, S., Luo, L., & Wynshaw-Boris, A. (2020). LIS1 determines cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.51512","ama":"Moon HM, Hippenmeyer S, Luo L, Wynshaw-Boris A. LIS1 determines cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility. eLife. 2020;9. doi:10.7554/elife.51512","short":"H.M. Moon, S. Hippenmeyer, L. Luo, A. Wynshaw-Boris, ELife 9 (2020).","ieee":"H. M. Moon, S. Hippenmeyer, L. Luo, and A. Wynshaw-Boris, “LIS1 determines cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility,” eLife, vol. 9. eLife Sciences Publications, 2020.","chicago":"Moon, Hyang Mi, Simon Hippenmeyer, Liqun Luo, and Anthony Wynshaw-Boris. “LIS1 Determines Cleavage Plane Positioning by Regulating Actomyosin-Mediated Cell Membrane Contractility.” ELife. eLife Sciences Publications, 2020. https://doi.org/10.7554/elife.51512.","ista":"Moon HM, Hippenmeyer S, Luo L, Wynshaw-Boris A. 2020. LIS1 determines cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility. eLife. 9, 51512."},"article_number":"51512","date_created":"2020-03-20T13:16:41Z","doi":"10.7554/elife.51512","date_published":"2020-03-11T00:00:00Z","publication":"eLife","day":"11","year":"2020","isi":1,"has_accepted_license":"1","oa":1,"quality_controlled":"1","publisher":"eLife Sciences Publications","department":[{"_id":"SiHi"}],"file_date_updated":"2020-09-24T07:03:20Z","ddc":["570"],"date_updated":"2023-08-18T07:06:31Z","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","_id":"7593","volume":9,"language":[{"iso":"eng"}],"file":[{"creator":"dernst","file_size":15089438,"date_updated":"2020-09-24T07:03:20Z","file_name":"2020_elife_Moon.pdf","date_created":"2020-09-24T07:03:20Z","relation":"main_file","access_level":"open_access","content_type":"application/pdf","success":1,"file_id":"8567","checksum":"396ceb2dd10b102ef4e699666b9342c3"}],"publication_status":"published","publication_identifier":{"issn":["2050-084X"]},"intvolume":" 9","month":"03","main_file_link":[{"url":"https://doi.org/10.1101/751958","open_access":"1"}],"scopus_import":"1","oa_version":"Published Version","pmid":1,"abstract":[{"lang":"eng","text":"Heterozygous loss of human PAFAH1B1 (coding for LIS1) results in the disruption of neurogenesis and neuronal migration via dysregulation of microtubule (MT) stability and dynein motor function/localization that alters mitotic spindle orientation, chromosomal segregation, and nuclear migration. Recently, human induced pluripotent stem cell (iPSC) models revealed an important role for LIS1 in controlling the length of terminal cell divisions of outer radial glial (oRG) progenitors, suggesting cellular functions of LIS1 in regulating neural progenitor cell (NPC) daughter cell separation. Here we examined the late mitotic stages NPCs in vivo and mouse embryonic fibroblasts (MEFs) in vitro from Pafah1b1-deficient mutants. Pafah1b1-deficient neocortical NPCs and MEFs similarly exhibited cleavage plane displacement with mislocalization of furrow-associated markers, associated with actomyosin dysfunction and cell membrane hyper-contractility. Thus, it suggests LIS1 acts as a key molecular link connecting MTs/dynein and actomyosin, ensuring that cell membrane contractility is tightly controlled to execute proper daughter cell separation."}]},{"publisher":"Springer Nature","quality_controlled":"1","oa":1,"acknowledgement":"The authors would like to thank A. van Lierop for technical assistance. In addition, we thank C. Dullin, J. Missbach-Güntner and S. Greco for advice and assistance with fpVCT imaging. Furthermore, the authors would like to thank H. K. Horst for advice on performing matrigel plug assays. This study has also been partially presented in A. Schorr’s doctoral thesis and the funding report of the SPP 1190 ‘The tumor-vessel interface’ of the ‘Deutsche Forschungsgemeinschaft’ (DFG).\r\nThis project was funded by the SPP 1190 “The tumor-vessel interface” and HO 2092/8-1 of the ‘Deutsche Forschungsgemeinschaft’ (DFG) to B. Homey. In addition, it was supported by grants from the Austrian Science Fund (FWF, W1212 to N. Amberg and J. Klufa and I4300-B to T. Bauer), the WWTF project LS16-025 and the European Research Council (ERC) Advanced grant (ERC-2015-AdG TNT-Tumors 694883) to M. Sibilia.","doi":"10.1038/s41416-020-0943-2","date_published":"2020-09-15T00:00:00Z","date_created":"2020-07-05T22:00:46Z","page":"942-954","day":"15","publication":"British Journal of Cancer","isi":1,"has_accepted_license":"1","year":"2020","title":"EGFR/Ras-induced CCL20 production modulates the tumour microenvironment","author":[{"last_name":"Hippe","full_name":"Hippe, Andreas","first_name":"Andreas"},{"full_name":"Braun, Stephan Alexander","last_name":"Braun","first_name":"Stephan Alexander"},{"first_name":"Péter","last_name":"Oláh","full_name":"Oláh, Péter"},{"full_name":"Gerber, Peter Arne","last_name":"Gerber","first_name":"Peter Arne"},{"first_name":"Anne","full_name":"Schorr, Anne","last_name":"Schorr"},{"first_name":"Stephan","full_name":"Seeliger, Stephan","last_name":"Seeliger"},{"last_name":"Holtz","full_name":"Holtz, Stephanie","first_name":"Stephanie"},{"first_name":"Katharina","last_name":"Jannasch","full_name":"Jannasch, Katharina"},{"full_name":"Pivarcsi, Andor","last_name":"Pivarcsi","first_name":"Andor"},{"first_name":"Bettina","last_name":"Buhren","full_name":"Buhren, Bettina"},{"first_name":"Holger","full_name":"Schrumpf, Holger","last_name":"Schrumpf"},{"first_name":"Andreas","last_name":"Kislat","full_name":"Kislat, Andreas"},{"last_name":"Bünemann","full_name":"Bünemann, Erich","first_name":"Erich"},{"first_name":"Martin","full_name":"Steinhoff, Martin","last_name":"Steinhoff"},{"last_name":"Fischer","full_name":"Fischer, Jens","first_name":"Jens"},{"last_name":"Lira","full_name":"Lira, Sérgio A.","first_name":"Sérgio A."},{"first_name":"Petra","full_name":"Boukamp, Petra","last_name":"Boukamp"},{"first_name":"Peter","last_name":"Hevezi","full_name":"Hevezi, Peter"},{"first_name":"Nikolas Hendrik","last_name":"Stoecklein","full_name":"Stoecklein, Nikolas Hendrik"},{"full_name":"Hoffmann, Thomas","last_name":"Hoffmann","first_name":"Thomas"},{"first_name":"Frauke","full_name":"Alves, Frauke","last_name":"Alves"},{"full_name":"Sleeman, Jonathan","last_name":"Sleeman","first_name":"Jonathan"},{"last_name":"Bauer","full_name":"Bauer, Thomas","first_name":"Thomas"},{"last_name":"Klufa","full_name":"Klufa, Jörg","first_name":"Jörg"},{"orcid":"0000-0002-3183-8207","full_name":"Amberg, Nicole","last_name":"Amberg","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","first_name":"Nicole"},{"last_name":"Sibilia","full_name":"Sibilia, Maria","first_name":"Maria"},{"last_name":"Zlotnik","full_name":"Zlotnik, Albert","first_name":"Albert"},{"first_name":"Anja","last_name":"Müller-Homey","full_name":"Müller-Homey, Anja"},{"full_name":"Homey, Bernhard","last_name":"Homey","first_name":"Bernhard"}],"article_processing_charge":"No","external_id":{"pmid":["32601464"],"isi":["000544152500001"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"mla":"Hippe, Andreas, et al. “EGFR/Ras-Induced CCL20 Production Modulates the Tumour Microenvironment.” British Journal of Cancer, vol. 123, Springer Nature, 2020, pp. 942–54, doi:10.1038/s41416-020-0943-2.","short":"A. Hippe, S.A. Braun, P. Oláh, P.A. Gerber, A. Schorr, S. Seeliger, S. Holtz, K. Jannasch, A. Pivarcsi, B. Buhren, H. Schrumpf, A. Kislat, E. Bünemann, M. Steinhoff, J. Fischer, S.A. Lira, P. Boukamp, P. Hevezi, N.H. Stoecklein, T. Hoffmann, F. Alves, J. Sleeman, T. Bauer, J. Klufa, N. Amberg, M. Sibilia, A. Zlotnik, A. Müller-Homey, B. Homey, British Journal of Cancer 123 (2020) 942–954.","ieee":"A. Hippe et al., “EGFR/Ras-induced CCL20 production modulates the tumour microenvironment,” British Journal of Cancer, vol. 123. Springer Nature, pp. 942–954, 2020.","ama":"Hippe A, Braun SA, Oláh P, et al. EGFR/Ras-induced CCL20 production modulates the tumour microenvironment. British Journal of Cancer. 2020;123:942-954. doi:10.1038/s41416-020-0943-2","apa":"Hippe, A., Braun, S. A., Oláh, P., Gerber, P. A., Schorr, A., Seeliger, S., … Homey, B. (2020). EGFR/Ras-induced CCL20 production modulates the tumour microenvironment. British Journal of Cancer. Springer Nature. https://doi.org/10.1038/s41416-020-0943-2","chicago":"Hippe, Andreas, Stephan Alexander Braun, Péter Oláh, Peter Arne Gerber, Anne Schorr, Stephan Seeliger, Stephanie Holtz, et al. “EGFR/Ras-Induced CCL20 Production Modulates the Tumour Microenvironment.” British Journal of Cancer. Springer Nature, 2020. https://doi.org/10.1038/s41416-020-0943-2.","ista":"Hippe A, Braun SA, Oláh P, Gerber PA, Schorr A, Seeliger S, Holtz S, Jannasch K, Pivarcsi A, Buhren B, Schrumpf H, Kislat A, Bünemann E, Steinhoff M, Fischer J, Lira SA, Boukamp P, Hevezi P, Stoecklein NH, Hoffmann T, Alves F, Sleeman J, Bauer T, Klufa J, Amberg N, Sibilia M, Zlotnik A, Müller-Homey A, Homey B. 2020. EGFR/Ras-induced CCL20 production modulates the tumour microenvironment. British Journal of Cancer. 123, 942–954."},"month":"09","intvolume":" 123","scopus_import":"1","oa_version":"Published Version","pmid":1,"abstract":[{"lang":"eng","text":"Background: The activation of the EGFR/Ras-signalling pathway in tumour cells induces a distinct chemokine repertoire, which in turn modulates the tumour microenvironment.\r\nMethods: The effects of EGFR/Ras on the expression and translation of CCL20 were analysed in a large set of epithelial cancer cell lines and tumour tissues by RT-qPCR and ELISA in vitro. CCL20 production was verified by immunohistochemistry in different tumour tissues and correlated with clinical data. The effects of CCL20 on endothelial cell migration and tumour-associated vascularisation were comprehensively analysed with chemotaxis assays in vitro and in CCR6-deficient mice in vivo.\r\nResults: Tumours facilitate progression by the EGFR/Ras-induced production of CCL20. Expression of the chemokine CCL20 in tumours correlates with advanced tumour stage, increased lymph node metastasis and decreased survival in patients. Microvascular endothelial cells abundantly express the specific CCL20 receptor CCR6. CCR6 signalling in endothelial cells induces angiogenesis. CCR6-deficient mice show significantly decreased tumour growth and tumour-associated vascularisation. The observed phenotype is dependent on CCR6 deficiency in stromal cells but not within the immune system.\r\nConclusion: We propose that the chemokine axis CCL20–CCR6 represents a novel and promising target to interfere with the tumour microenvironment, and opens an innovative multimodal strategy for cancer therapy."}],"volume":123,"related_material":{"record":[{"id":"10170","status":"deleted","relation":"later_version"}],"link":[{"url":"https://doi.org/10.1038/s41416-021-01563-y","relation":"erratum"}]},"file":[{"success":1,"checksum":"05a8e65d49c3f5b8e37ac4afe68287e2","file_id":"10398","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_name":"2020_BrJournalCancer_Hippe.pdf","date_created":"2021-12-02T12:35:12Z","file_size":3620691,"date_updated":"2021-12-02T12:35:12Z","creator":"cchlebak"}],"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["1532-1827"],"issn":["0007-0920"]},"publication_status":"published","status":"public","type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"8093","department":[{"_id":"SiHi"}],"file_date_updated":"2021-12-02T12:35:12Z","ddc":["610"],"date_updated":"2023-08-22T07:51:12Z"},{"citation":{"chicago":"Laukoter, Susanne, Florian Pauler, Robert J Beattie, Nicole Amberg, Andi H Hansen, Carmen Streicher, Thomas Penz, Christoph Bock, and Simon Hippenmeyer. “Cell-Type Specificity of Genomic Imprinting in Cerebral Cortex.” Neuron. Elsevier, 2020. https://doi.org/10.1016/j.neuron.2020.06.031.","ista":"Laukoter S, Pauler F, Beattie RJ, Amberg N, Hansen AH, Streicher C, Penz T, Bock C, Hippenmeyer S. 2020. Cell-type specificity of genomic imprinting in cerebral cortex. Neuron. 107(6), 1160–1179.e9.","mla":"Laukoter, Susanne, et al. “Cell-Type Specificity of Genomic Imprinting in Cerebral Cortex.” Neuron, vol. 107, no. 6, Elsevier, 2020, p. 1160–1179.e9, doi:10.1016/j.neuron.2020.06.031.","ieee":"S. Laukoter et al., “Cell-type specificity of genomic imprinting in cerebral cortex,” Neuron, vol. 107, no. 6. Elsevier, p. 1160–1179.e9, 2020.","short":"S. Laukoter, F. Pauler, R.J. Beattie, N. Amberg, A.H. Hansen, C. Streicher, T. Penz, C. Bock, S. Hippenmeyer, Neuron 107 (2020) 1160–1179.e9.","apa":"Laukoter, S., Pauler, F., Beattie, R. J., Amberg, N., Hansen, A. H., Streicher, C., … Hippenmeyer, S. (2020). Cell-type specificity of genomic imprinting in cerebral cortex. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2020.06.031","ama":"Laukoter S, Pauler F, Beattie RJ, et al. Cell-type specificity of genomic imprinting in cerebral cortex. Neuron. 2020;107(6):1160-1179.e9. doi:10.1016/j.neuron.2020.06.031"},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","author":[{"orcid":"0000-0002-7903-3010","full_name":"Laukoter, Susanne","last_name":"Laukoter","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","first_name":"Susanne"},{"orcid":"0000-0002-7462-0048","full_name":"Pauler, Florian","last_name":"Pauler","first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","first_name":"Robert J","orcid":"0000-0002-8483-8753","full_name":"Beattie, Robert J","last_name":"Beattie"},{"id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","first_name":"Nicole","last_name":"Amberg","orcid":"0000-0002-3183-8207","full_name":"Amberg, Nicole"},{"last_name":"Hansen","full_name":"Hansen, Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87","first_name":"Andi H"},{"id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","first_name":"Carmen","last_name":"Streicher","full_name":"Streicher, Carmen"},{"full_name":"Penz, Thomas","last_name":"Penz","first_name":"Thomas"},{"first_name":"Christoph","last_name":"Bock","orcid":"0000-0001-6091-3088","full_name":"Bock, Christoph"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer"}],"external_id":{"isi":["000579698700006"]},"article_processing_charge":"No","title":"Cell-type specificity of genomic imprinting in cerebral cortex","project":[{"_id":"2625A13E-B435-11E9-9278-68D0E5697425","name":"Molecular Mechanisms of Radial Neuronal Migration","grant_number":"24812"},{"name":"Role of Eed in neural stem cell lineage progression","grant_number":"T0101031","call_identifier":"FWF","_id":"268F8446-B435-11E9-9278-68D0E5697425"},{"_id":"264E56E2-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex","grant_number":"M02416"},{"name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain","grant_number":"LS13-002","_id":"25D92700-B435-11E9-9278-68D0E5697425"},{"grant_number":"RGP0053/2014","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level","_id":"25D7962E-B435-11E9-9278-68D0E5697425"},{"grant_number":"618444","name":"Molecular Mechanisms of Cerebral Cortex Development","call_identifier":"FP7","_id":"25D61E48-B435-11E9-9278-68D0E5697425"},{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}],"isi":1,"has_accepted_license":"1","year":"2020","day":"23","publication":"Neuron","page":"1160-1179.e9","date_published":"2020-09-23T00:00:00Z","doi":"10.1016/j.neuron.2020.06.031","date_created":"2020-07-23T16:03:12Z","acknowledgement":"We thank A. Heger (IST Austria Preclinical Facility), A. Sommer and C. Czepe (VBCF GmbH, NGS Unit), and A. Seitz and P. Moll (Lexogen GmbH) for technical support; G. Arque, S. Resch, C. Igler, C. Dotter, C. Yahya, Q. Hudson, and D. Andergassen for initial experiments and/or assistance; D. Barlow, O. Bell, and all members of the Hippenmeyer lab for discussion; and N. Barton, B. Vicoso, M. Sixt, and L. Luo for comments on earlier versions of the manuscript. This research was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Bioimaging Facilities (BIF), Life Science Facilities (LSF), and Preclinical Facilities (PCF). A.H.H. is a recipient of a DOC fellowship (24812) of the Austrian Academy of Sciences. N.A. received support from the FWF Firnberg-Programm (T 1031). R.B. received support from the FWF Meitner-Programm (M 2416). This work was also supported by IST Austria institutional funds; a NÖ Forschung und Bildung n[f+b] life science call grant (C13-002) to S.H.; a program grant from the Human Frontiers Science Program (RGP0053/2014) to S.H.; the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement 618444 to S.H.; and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program (grant agreement 725780 LinPro) to S.H.","quality_controlled":"1","publisher":"Elsevier","oa":1,"date_updated":"2023-08-22T08:20:11Z","ddc":["570"],"file_date_updated":"2020-12-02T09:26:46Z","department":[{"_id":"SiHi"}],"_id":"8162","article_type":"original","type":"journal_article","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"status":"public","publication_identifier":{"issn":["0896-6273"]},"publication_status":"published","file":[{"file_id":"8828","checksum":"7becdc16a6317304304631087ae7dd7f","success":1,"content_type":"application/pdf","access_level":"open_access","relation":"main_file","date_created":"2020-12-02T09:26:46Z","file_name":"2020_Neuron_Laukoter.pdf","date_updated":"2020-12-02T09:26:46Z","file_size":8911830,"creator":"dernst"}],"language":[{"iso":"eng"}],"issue":"6","related_material":{"link":[{"url":"https://ist.ac.at/en/news/cells-react-differently-to-genomic-imprinting/","relation":"press_release","description":"News on IST Website"}]},"volume":107,"ec_funded":1,"acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"},{"_id":"PreCl"}],"abstract":[{"text":"In mammalian genomes, a subset of genes is regulated by genomic imprinting, resulting in silencing of one parental allele. Imprinting is essential for cerebral cortex development, but prevalence and functional impact in individual cells is unclear. Here, we determined allelic expression in cortical cell types and established a quantitative platform to interrogate imprinting in single cells. We created cells with uniparental chromosome disomy (UPD) containing two copies of either the maternal or the paternal chromosome; hence, imprinted genes will be 2-fold overexpressed or not expressed. By genetic labeling of UPD, we determined cellular phenotypes and transcriptional responses to deregulated imprinted gene expression at unprecedented single-cell resolution. We discovered an unexpected degree of cell-type specificity and a novel function of imprinting in the regulation of cortical astrocyte survival. More generally, our results suggest functional relevance of imprinted gene expression in glial astrocyte lineage and thus for generating cortical cell-type diversity.","lang":"eng"}],"oa_version":"Published Version","scopus_import":"1","month":"09","intvolume":" 107"},{"publisher":"Wiley","quality_controlled":"1","oa":1,"acknowledgement":"The authors thank Drs. J. Eisen, QR. Lu, S. Duan, Z‐H. Li, W. Mo, and Q. Wu for their critical comments on the manuscript. They also thank Dr. H. Zong for providing the CKO_NG2‐CreER model. This work is supported by the National Key Research and Development Program of China, Stem Cell and Translational Research (2016YFA0101201 to C.L., 2016YFA0100303 to Y.J.W.), the National Natural Science Foundation of China (81673035 and 81972915 to C.L., 81472722 to Y.J.W.), the Science Foundation for Distinguished Young Scientists of Zhejiang Province (LR17H160001 to C.L.), Fundamental Research Funds for the Central Universities (2016QNA7023 and 2017QNA7028 to C.L.) and the Thousand Talent Program for Young Outstanding Scientists, China (to C.L.), IST Austria institutional funds (to S.H.), European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (725780 LinPro to S.H.). C.L. is a scholar of K. C. Wong Education Foundation.","doi":"10.1002/advs.202001724","date_published":"2020-11-04T00:00:00Z","date_created":"2020-10-01T09:44:13Z","day":"04","publication":"Advanced Science","has_accepted_license":"1","isi":1,"year":"2020","project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}],"article_number":"2001724","title":"Oncogenic state and cell identity combinatorially dictate the susceptibility of cells within glioma development hierarchy to IGF1R targeting","author":[{"first_name":"Anhao","full_name":"Tian, Anhao","last_name":"Tian"},{"last_name":"Kang","full_name":"Kang, Bo","first_name":"Bo"},{"first_name":"Baizhou","last_name":"Li","full_name":"Li, Baizhou"},{"first_name":"Biying","full_name":"Qiu, Biying","last_name":"Qiu"},{"first_name":"Wenhong","last_name":"Jiang","full_name":"Jiang, Wenhong"},{"first_name":"Fangjie","last_name":"Shao","full_name":"Shao, Fangjie"},{"full_name":"Gao, Qingqing","last_name":"Gao","first_name":"Qingqing"},{"full_name":"Liu, Rui","last_name":"Liu","first_name":"Rui"},{"last_name":"Cai","full_name":"Cai, Chengwei","first_name":"Chengwei"},{"full_name":"Jing, Rui","last_name":"Jing","first_name":"Rui"},{"last_name":"Wang","full_name":"Wang, Wei","first_name":"Wei"},{"first_name":"Pengxiang","last_name":"Chen","full_name":"Chen, Pengxiang"},{"full_name":"Liang, Qinghui","last_name":"Liang","first_name":"Qinghui"},{"full_name":"Bao, Lili","last_name":"Bao","first_name":"Lili"},{"full_name":"Man, Jianghong","last_name":"Man","first_name":"Jianghong"},{"full_name":"Wang, Yan","last_name":"Wang","first_name":"Yan"},{"full_name":"Shi, Yu","last_name":"Shi","first_name":"Yu"},{"full_name":"Li, Jin","last_name":"Li","first_name":"Jin"},{"last_name":"Yang","full_name":"Yang, Minmin","first_name":"Minmin"},{"first_name":"Lisha","full_name":"Wang, Lisha","last_name":"Wang"},{"full_name":"Zhang, Jianmin","last_name":"Zhang","first_name":"Jianmin"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer"},{"full_name":"Zhu, Junming","last_name":"Zhu","first_name":"Junming"},{"last_name":"Bian","full_name":"Bian, Xiuwu","first_name":"Xiuwu"},{"first_name":"Ying‐Jie","last_name":"Wang","full_name":"Wang, Ying‐Jie"},{"full_name":"Liu, Chong","last_name":"Liu","first_name":"Chong"}],"external_id":{"isi":["000573860700001"]},"article_processing_charge":"No","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"chicago":"Tian, Anhao, Bo Kang, Baizhou Li, Biying Qiu, Wenhong Jiang, Fangjie Shao, Qingqing Gao, et al. “Oncogenic State and Cell Identity Combinatorially Dictate the Susceptibility of Cells within Glioma Development Hierarchy to IGF1R Targeting.” Advanced Science. Wiley, 2020. https://doi.org/10.1002/advs.202001724.","ista":"Tian A, Kang B, Li B, Qiu B, Jiang W, Shao F, Gao Q, Liu R, Cai C, Jing R, Wang W, Chen P, Liang Q, Bao L, Man J, Wang Y, Shi Y, Li J, Yang M, Wang L, Zhang J, Hippenmeyer S, Zhu J, Bian X, Wang Y, Liu C. 2020. Oncogenic state and cell identity combinatorially dictate the susceptibility of cells within glioma development hierarchy to IGF1R targeting. Advanced Science. 7(21), 2001724.","mla":"Tian, Anhao, et al. “Oncogenic State and Cell Identity Combinatorially Dictate the Susceptibility of Cells within Glioma Development Hierarchy to IGF1R Targeting.” Advanced Science, vol. 7, no. 21, 2001724, Wiley, 2020, doi:10.1002/advs.202001724.","short":"A. Tian, B. Kang, B. Li, B. Qiu, W. Jiang, F. Shao, Q. Gao, R. Liu, C. Cai, R. Jing, W. Wang, P. Chen, Q. Liang, L. Bao, J. Man, Y. Wang, Y. Shi, J. Li, M. Yang, L. Wang, J. Zhang, S. Hippenmeyer, J. Zhu, X. Bian, Y. Wang, C. Liu, Advanced Science 7 (2020).","ieee":"A. Tian et al., “Oncogenic state and cell identity combinatorially dictate the susceptibility of cells within glioma development hierarchy to IGF1R targeting,” Advanced Science, vol. 7, no. 21. Wiley, 2020.","ama":"Tian A, Kang B, Li B, et al. Oncogenic state and cell identity combinatorially dictate the susceptibility of cells within glioma development hierarchy to IGF1R targeting. Advanced Science. 2020;7(21). doi:10.1002/advs.202001724","apa":"Tian, A., Kang, B., Li, B., Qiu, B., Jiang, W., Shao, F., … Liu, C. (2020). Oncogenic state and cell identity combinatorially dictate the susceptibility of cells within glioma development hierarchy to IGF1R targeting. Advanced Science. Wiley. https://doi.org/10.1002/advs.202001724"},"month":"11","intvolume":" 7","oa_version":"Published Version","abstract":[{"text":"Glioblastoma is the most malignant cancer in the brain and currently incurable. It is urgent to identify effective targets for this lethal disease. Inhibition of such targets should suppress the growth of cancer cells and, ideally also precancerous cells for early prevention, but minimally affect their normal counterparts. Using genetic mouse models with neural stem cells (NSCs) or oligodendrocyte precursor cells (OPCs) as the cells‐of‐origin/mutation, it is shown that the susceptibility of cells within the development hierarchy of glioma to the knockout of insulin‐like growth factor I receptor (IGF1R) is determined not only by their oncogenic states, but also by their cell identities/states. Knockout of IGF1R selectively disrupts the growth of mutant and transformed, but not normal OPCs, or NSCs. The desirable outcome of IGF1R knockout on cell growth requires the mutant cells to commit to the OPC identity regardless of its development hierarchical status. At the molecular level, oncogenic mutations reprogram the cellular network of OPCs and force them to depend more on IGF1R for their growth. A new‐generation brain‐penetrable, orally available IGF1R inhibitor harnessing tumor OPCs in the brain is also developed. The findings reveal the cellular window of IGF1R targeting and establish IGF1R as an effective target for the prevention and treatment of glioblastoma.","lang":"eng"}],"issue":"21","volume":7,"ec_funded":1,"file":[{"relation":"main_file","access_level":"open_access","content_type":"application/pdf","success":1,"file_id":"8938","checksum":"92818c23ecc70e35acfa671f3cfb9909","creator":"dernst","file_size":7835833,"date_updated":"2020-12-10T14:07:24Z","file_name":"2020_AdvScience_Tian.pdf","date_created":"2020-12-10T14:07:24Z"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2198-3844"]},"publication_status":"published","status":"public","keyword":["General Engineering","General Physics and Astronomy","General Materials Science","Medicine (miscellaneous)","General Chemical Engineering","Biochemistry","Genetics and Molecular Biology (miscellaneous)"],"type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"8592","file_date_updated":"2020-12-10T14:07:24Z","department":[{"_id":"SiHi"}],"ddc":["570"],"date_updated":"2023-08-22T09:53:01Z"},{"_id":"8949","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","status":"public","date_updated":"2023-08-24T10:57:48Z","ddc":["570"],"department":[{"_id":"SiHi"}],"file_date_updated":"2020-12-14T08:09:43Z","abstract":[{"lang":"eng","text":"Development of the nervous system undergoes important transitions, including one from neurogenesis to gliogenesis which occurs late during embryonic gestation. Here we report on clonal analysis of gliogenesis in mice using Mosaic Analysis with Double Markers (MADM) with quantitative and computational methods. Results reveal that developmental gliogenesis in the cerebral cortex occurs in a fraction of earlier neurogenic clones, accelerating around E16.5, and giving rise to both astrocytes and oligodendrocytes. Moreover, MADM-based genetic deletion of the epidermal growth factor receptor (Egfr) in gliogenic clones revealed that Egfr is cell autonomously required for gliogenesis in the mouse dorsolateral cortices. A broad range in the proliferation capacity, symmetry of clones, and competitive advantage of MADM cells was evident in clones that contained one cellular lineage with double dosage of Egfr relative to their environment, while their sibling Egfr-null cells failed to generate glia. Remarkably, the total numbers of glia in MADM clones balance out regardless of significant alterations in clonal symmetries. The variability in glial clones shows stochastic patterns that we define mathematically, which are different from the deterministic patterns in neuronal clones. This study sets a foundation for studying the biological significance of stochastic and deterministic clonal principles underlying tissue development, and identifying mechanisms that differentiate between neurogenesis and gliogenesis."}],"oa_version":"Published Version","intvolume":" 9","month":"12","publication_status":"published","publication_identifier":{"issn":["2073-4409"]},"language":[{"iso":"eng"}],"file":[{"success":1,"checksum":"5095cbdc728c9a510c5761cf60a8861c","file_id":"8950","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_name":"2020_Cells_Zhang.pdf","date_created":"2020-12-14T08:09:43Z","file_size":3504525,"date_updated":"2020-12-14T08:09:43Z","creator":"dernst"}],"ec_funded":1,"volume":9,"issue":"12","article_number":"2662","project":[{"grant_number":"M02416","name":"Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex","call_identifier":"FWF","_id":"264E56E2-B435-11E9-9278-68D0E5697425"},{"call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780"}],"citation":{"ama":"Zhang X, Mennicke CV, Xiao G, et al. Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage. Cells. 2020;9(12). doi:10.3390/cells9122662","apa":"Zhang, X., Mennicke, C. V., Xiao, G., Beattie, R. J., Haider, M., Hippenmeyer, S., & Ghashghaei, H. T. (2020). Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage. Cells. MDPI. https://doi.org/10.3390/cells9122662","short":"X. Zhang, C.V. Mennicke, G. Xiao, R.J. Beattie, M. Haider, S. Hippenmeyer, H.T. Ghashghaei, Cells 9 (2020).","ieee":"X. Zhang et al., “Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage,” Cells, vol. 9, no. 12. MDPI, 2020.","mla":"Zhang, Xuying, et al. “Clonal Analysis of Gliogenesis in the Cerebral Cortex Reveals Stochastic Expansion of Glia and Cell Autonomous Responses to Egfr Dosage.” Cells, vol. 9, no. 12, 2662, MDPI, 2020, doi:10.3390/cells9122662.","ista":"Zhang X, Mennicke CV, Xiao G, Beattie RJ, Haider M, Hippenmeyer S, Ghashghaei HT. 2020. Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage. Cells. 9(12), 2662.","chicago":"Zhang, Xuying, Christine V. Mennicke, Guanxi Xiao, Robert J Beattie, Mansoor Haider, Simon Hippenmeyer, and H. Troy Ghashghaei. “Clonal Analysis of Gliogenesis in the Cerebral Cortex Reveals Stochastic Expansion of Glia and Cell Autonomous Responses to Egfr Dosage.” Cells. MDPI, 2020. https://doi.org/10.3390/cells9122662."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","article_processing_charge":"No","external_id":{"isi":["000601787300001"]},"author":[{"first_name":"Xuying","last_name":"Zhang","full_name":"Zhang, Xuying"},{"first_name":"Christine V.","last_name":"Mennicke","full_name":"Mennicke, Christine V."},{"first_name":"Guanxi","last_name":"Xiao","full_name":"Xiao, Guanxi"},{"orcid":"0000-0002-8483-8753","full_name":"Beattie, Robert J","last_name":"Beattie","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","first_name":"Robert J"},{"first_name":"Mansoor","last_name":"Haider","full_name":"Haider, Mansoor"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon"},{"full_name":"Ghashghaei, H. Troy","last_name":"Ghashghaei","first_name":"H. Troy"}],"title":"Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage","acknowledgement":"This research was funded by grants from the National Institutes of Health to H.T.G. (R01NS098370 and R01NS089795). C.V.M. was supported by a National Science Foundation Graduate Research Fellowship (DGE-1746939). R.B. was supported by the FWF Lise-Meitner program (M 2416), and S.H. was supported by the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement No 725780 LinPro).The authors thank members of the Ghashghaei lab for discussions, technical support, and help with preparation of the manuscript.","oa":1,"publisher":"MDPI","quality_controlled":"1","year":"2020","has_accepted_license":"1","isi":1,"publication":"Cells","day":"11","date_created":"2020-12-14T08:04:03Z","date_published":"2020-12-11T00:00:00Z","doi":"10.3390/cells9122662"},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Santini, Laura, et al. “Novel Imprints in Mouse Blastocysts Are Predominantly DNA Methylation Independent.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2020.11.03.366948.","apa":"Santini, L., Halbritter, F., Titz-Teixeira, F., Suzuki, T., Asami, M., Ramesmayer, J., … Leeb, M. (n.d.). Novel imprints in mouse blastocysts are predominantly DNA methylation independent. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2020.11.03.366948","ama":"Santini L, Halbritter F, Titz-Teixeira F, et al. Novel imprints in mouse blastocysts are predominantly DNA methylation independent. bioRxiv. doi:10.1101/2020.11.03.366948","short":"L. Santini, F. Halbritter, F. Titz-Teixeira, T. Suzuki, M. Asami, J. Ramesmayer, X. Ma, A. Lackner, N. Warr, F. Pauler, S. Hippenmeyer, E. Laue, M. Farlik, C. Bock, A. Beyer, A.C.F. Perry, M. Leeb, BioRxiv (n.d.).","ieee":"L. Santini et al., “Novel imprints in mouse blastocysts are predominantly DNA methylation independent,” bioRxiv. Cold Spring Harbor Laboratory.","chicago":"Santini, Laura, Florian Halbritter, Fabian Titz-Teixeira, Toru Suzuki, Maki Asami, Julia Ramesmayer, Xiaoyan Ma, et al. “Novel Imprints in Mouse Blastocysts Are Predominantly DNA Methylation Independent.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2020.11.03.366948.","ista":"Santini L, Halbritter F, Titz-Teixeira F, Suzuki T, Asami M, Ramesmayer J, Ma X, Lackner A, Warr N, Pauler F, Hippenmeyer S, Laue E, Farlik M, Bock C, Beyer A, Perry ACF, Leeb M. Novel imprints in mouse blastocysts are predominantly DNA methylation independent. bioRxiv, 10.1101/2020.11.03.366948."},"date_updated":"2023-09-12T11:05:28Z","title":"Novel imprints in mouse blastocysts are predominantly DNA methylation independent","department":[{"_id":"SiHi"}],"article_processing_charge":"No","external_id":{"pmid":["PPR234457 "]},"author":[{"first_name":"Laura","last_name":"Santini","full_name":"Santini, Laura"},{"last_name":"Halbritter","full_name":"Halbritter, Florian","first_name":"Florian"},{"first_name":"Fabian","last_name":"Titz-Teixeira","full_name":"Titz-Teixeira, Fabian"},{"last_name":"Suzuki","full_name":"Suzuki, Toru","first_name":"Toru"},{"last_name":"Asami","full_name":"Asami, Maki","first_name":"Maki"},{"last_name":"Ramesmayer","full_name":"Ramesmayer, Julia","first_name":"Julia"},{"first_name":"Xiaoyan","full_name":"Ma, Xiaoyan","last_name":"Ma"},{"last_name":"Lackner","full_name":"Lackner, Andreas","first_name":"Andreas"},{"first_name":"Nick","full_name":"Warr, Nick","last_name":"Warr"},{"full_name":"Pauler, Florian","orcid":"0000-0002-7462-0048","last_name":"Pauler","first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"},{"last_name":"Laue","full_name":"Laue, Ernest","first_name":"Ernest"},{"last_name":"Farlik","full_name":"Farlik, Matthias","first_name":"Matthias"},{"full_name":"Bock, Christoph","last_name":"Bock","first_name":"Christoph"},{"first_name":"Andreas","last_name":"Beyer","full_name":"Beyer, Andreas"},{"last_name":"Perry","full_name":"Perry, Anthony C. F.","first_name":"Anthony C. F."},{"first_name":"Martin","full_name":"Leeb, Martin","last_name":"Leeb"}],"_id":"8813","status":"public","type":"preprint","publication":"bioRxiv","language":[{"iso":"eng"}],"day":"05","year":"2020","publication_status":"submitted","date_created":"2020-11-26T07:17:19Z","date_published":"2020-11-05T00:00:00Z","doi":"10.1101/2020.11.03.366948","oa_version":"Preprint","pmid":1,"abstract":[{"text":"In mammals, chromatin marks at imprinted genes are asymmetrically inherited to control parentally-biased gene expression. This control is thought predominantly to involve parent-specific differentially methylated regions (DMR) in genomic DNA. However, neither parent-of-origin-specific transcription nor DMRs have been comprehensively mapped. We here address this by integrating transcriptomic and epigenomic approaches in mouse preimplantation embryos (blastocysts). Transcriptome-analysis identified 71 genes expressed with previously unknown parent-of-origin-specific expression in blastocysts (nBiX: novel blastocyst-imprinted expression). Uniparental expression of nBiX genes disappeared soon after implantation. Micro-whole-genome bisulfite sequencing (μWGBS) of individual uniparental blastocysts detected 859 DMRs. Only 18% of nBiXs were associated with a DMR, whereas 60% were associated with parentally-biased H3K27me3. This suggests a major role for Polycomb-mediated imprinting in blastocysts. Five nBiX-clusters contained at least one known imprinted gene, and five novel clusters contained exclusively nBiX-genes. These data suggest a complex program of stage-specific imprinting involving different tiers of regulation.","lang":"eng"}],"month":"11","main_file_link":[{"url":"https://doi.org/10.1101/2020.11.03.366948","open_access":"1"}],"oa":1,"publisher":"Cold Spring Harbor Laboratory"},{"pmid":1,"oa_version":"Published Version","abstract":[{"text":"Concerted radial migration of newly born cortical projection neurons, from their birthplace to their final target lamina, is a key step in the assembly of the cerebral cortex. The cellular and molecular mechanisms regulating the specific sequential steps of radial neuronal migration in vivo are however still unclear, let alone the effects and interactions with the extracellular environment. In any in vivo context, cells will always be exposed to a complex extracellular environment consisting of (1) secreted factors acting as potential signaling cues, (2) the extracellular matrix, and (3) other cells providing cell–cell interaction through receptors and/or direct physical stimuli. Most studies so far have described and focused mainly on intrinsic cell-autonomous gene functions in neuronal migration but there is accumulating evidence that non-cell-autonomous-, local-, systemic-, and/or whole tissue-wide effects substantially contribute to the regulation of radial neuronal migration. These non-cell-autonomous effects may differentially affect cortical neuron migration in distinct cellular environments. However, the cellular and molecular natures of such non-cell-autonomous mechanisms are mostly unknown. Furthermore, physical forces due to collective migration and/or community effects (i.e., interactions with surrounding cells) may play important roles in neocortical projection neuron migration. In this concise review, we first outline distinct models of non-cell-autonomous interactions of cortical projection neurons along their radial migration trajectory during development. We then summarize experimental assays and platforms that can be utilized to visualize and potentially probe non-cell-autonomous mechanisms. Lastly, we define key questions to address in the future.","lang":"eng"}],"intvolume":" 8","month":"09","scopus_import":"1","language":[{"iso":"eng"}],"file":[{"file_name":"2020_Frontiers_Hansen.pdf","date_created":"2020-09-28T13:11:17Z","creator":"dernst","file_size":5527139,"date_updated":"2020-09-28T13:11:17Z","success":1,"file_id":"8584","checksum":"01f731824194c94c81a5da360d997073","relation":"main_file","access_level":"open_access","content_type":"application/pdf"}],"publication_status":"published","publication_identifier":{"issn":["2296-634X"]},"ec_funded":1,"issue":"9","volume":8,"related_material":{"record":[{"status":"public","id":"9962","relation":"dissertation_contains"}]},"_id":"8569","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","ddc":["570"],"date_updated":"2024-03-27T23:30:40Z","file_date_updated":"2020-09-28T13:11:17Z","department":[{"_id":"SiHi"}],"acknowledgement":"AH was a recipient of a DOC Fellowship (24812) of the Austrian Academy of Sciences. This work also received support from IST Austria institutional funds; the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007–2013) under REA Grant Agreement No. 618444 to SH.","oa":1,"quality_controlled":"1","publisher":"Frontiers","publication":"Frontiers in Cell and Developmental Biology","day":"25","year":"2020","has_accepted_license":"1","isi":1,"date_created":"2020-09-26T06:11:07Z","doi":"10.3389/fcell.2020.574382","date_published":"2020-09-25T00:00:00Z","article_number":"574382","project":[{"_id":"2625A13E-B435-11E9-9278-68D0E5697425","name":"Molecular Mechanisms of Radial Neuronal Migration","grant_number":"24812"},{"grant_number":"618444","name":"Molecular Mechanisms of Cerebral Cortex Development","_id":"25D61E48-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"short":"A.H. Hansen, S. Hippenmeyer, Frontiers in Cell and Developmental Biology 8 (2020).","ieee":"A. H. Hansen and S. Hippenmeyer, “Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex,” Frontiers in Cell and Developmental Biology, vol. 8, no. 9. Frontiers, 2020.","apa":"Hansen, A. H., & Hippenmeyer, S. (2020). Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental Biology. Frontiers. https://doi.org/10.3389/fcell.2020.574382","ama":"Hansen AH, Hippenmeyer S. Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental Biology. 2020;8(9). doi:10.3389/fcell.2020.574382","mla":"Hansen, Andi H., and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms in Radial Projection Neuron Migration in the Developing Cerebral Cortex.” Frontiers in Cell and Developmental Biology, vol. 8, no. 9, 574382, Frontiers, 2020, doi:10.3389/fcell.2020.574382.","ista":"Hansen AH, Hippenmeyer S. 2020. Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental Biology. 8(9), 574382.","chicago":"Hansen, Andi H, and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms in Radial Projection Neuron Migration in the Developing Cerebral Cortex.” Frontiers in Cell and Developmental Biology. Frontiers, 2020. https://doi.org/10.3389/fcell.2020.574382."},"title":"Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex","article_processing_charge":"Yes (via OA deal)","external_id":{"isi":["000577915900001"],"pmid":["33102480"]},"author":[{"last_name":"Hansen","full_name":"Hansen, Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87","first_name":"Andi H"},{"last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}]},{"quality_controlled":"1","publisher":"MyJove Corporation","oa":1,"date_published":"2020-05-08T00:00:00Z","doi":"10.3791/61147","date_created":"2020-05-11T08:31:20Z","isi":1,"has_accepted_license":"1","year":"2020","day":"08","publication":"Journal of Visual Experiments","project":[{"call_identifier":"FWF","_id":"264E56E2-B435-11E9-9278-68D0E5697425","grant_number":"M02416","name":"Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex"},{"_id":"268F8446-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"T0101031","name":"Role of Eed in neural stem cell lineage progression"},{"name":"ISTplus - Postdoctoral Fellowships","grant_number":"754411","call_identifier":"H2020","_id":"260C2330-B435-11E9-9278-68D0E5697425"},{"name":"Molecular Mechanisms of Radial Neuronal Migration","grant_number":"24812","_id":"2625A13E-B435-11E9-9278-68D0E5697425"},{"_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780"}],"article_number":"e61147","author":[{"full_name":"Beattie, Robert J","orcid":"0000-0002-8483-8753","last_name":"Beattie","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","first_name":"Robert J"},{"last_name":"Streicher","full_name":"Streicher, Carmen","first_name":"Carmen","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Amberg","full_name":"Amberg, Nicole","orcid":"0000-0002-3183-8207","first_name":"Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87"},{"id":"471195F6-F248-11E8-B48F-1D18A9856A87","first_name":"Giselle T","full_name":"Cheung, Giselle T","orcid":"0000-0001-8457-2572","last_name":"Cheung"},{"full_name":"Contreras, Ximena","last_name":"Contreras","id":"475990FE-F248-11E8-B48F-1D18A9856A87","first_name":"Ximena"},{"full_name":"Hansen, Andi H","last_name":"Hansen","id":"38853E16-F248-11E8-B48F-1D18A9856A87","first_name":"Andi H"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"}],"article_processing_charge":"No","external_id":{"isi":["000546406600043"]},"title":"Lineage tracing and clonal analysis in developing cerebral cortex using mosaic analysis with double markers (MADM)","citation":{"mla":"Beattie, Robert J., et al. “Lineage Tracing and Clonal Analysis in Developing Cerebral Cortex Using Mosaic Analysis with Double Markers (MADM).” Journal of Visual Experiments, no. 159, e61147, MyJove Corporation, 2020, doi:10.3791/61147.","short":"R.J. Beattie, C. Streicher, N. Amberg, G.T. Cheung, X. Contreras, A.H. Hansen, S. Hippenmeyer, Journal of Visual Experiments (2020).","ieee":"R. J. Beattie et al., “Lineage tracing and clonal analysis in developing cerebral cortex using mosaic analysis with double markers (MADM),” Journal of Visual Experiments, no. 159. MyJove Corporation, 2020.","apa":"Beattie, R. J., Streicher, C., Amberg, N., Cheung, G. T., Contreras, X., Hansen, A. H., & Hippenmeyer, S. (2020). Lineage tracing and clonal analysis in developing cerebral cortex using mosaic analysis with double markers (MADM). Journal of Visual Experiments. MyJove Corporation. https://doi.org/10.3791/61147","ama":"Beattie RJ, Streicher C, Amberg N, et al. Lineage tracing and clonal analysis in developing cerebral cortex using mosaic analysis with double markers (MADM). Journal of Visual Experiments. 2020;(159). doi:10.3791/61147","chicago":"Beattie, Robert J, Carmen Streicher, Nicole Amberg, Giselle T Cheung, Ximena Contreras, Andi H Hansen, and Simon Hippenmeyer. “Lineage Tracing and Clonal Analysis in Developing Cerebral Cortex Using Mosaic Analysis with Double Markers (MADM).” Journal of Visual Experiments. MyJove Corporation, 2020. https://doi.org/10.3791/61147.","ista":"Beattie RJ, Streicher C, Amberg N, Cheung GT, Contreras X, Hansen AH, Hippenmeyer S. 2020. Lineage tracing and clonal analysis in developing cerebral cortex using mosaic analysis with double markers (MADM). Journal of Visual Experiments. (159), e61147."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","scopus_import":"1","month":"05","acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"},{"_id":"PreCl"}],"abstract":[{"text":"Beginning from a limited pool of progenitors, the mammalian cerebral cortex forms highly organized functional neural circuits. However, the underlying cellular and molecular mechanisms regulating lineage transitions of neural stem cells (NSCs) and eventual production of neurons and glia in the developing neuroepithelium remains unclear. Methods to trace NSC division patterns and map the lineage of clonally related cells have advanced dramatically. However, many contemporary lineage tracing techniques suffer from the lack of cellular resolution of progeny cell fate, which is essential for deciphering progenitor cell division patterns. Presented is a protocol using mosaic analysis with double markers (MADM) to perform in vivo clonal analysis. MADM concomitantly manipulates individual progenitor cells and visualizes precise division patterns and lineage progression at unprecedented single cell resolution. MADM-based interchromosomal recombination events during the G2-X phase of mitosis, together with temporally inducible CreERT2, provide exact information on the birth dates of clones and their division patterns. Thus, MADM lineage tracing provides unprecedented qualitative and quantitative optical readouts of the proliferation mode of stem cell progenitors at the single cell level. MADM also allows for examination of the mechanisms and functional requirements of candidate genes in NSC lineage progression. This method is unique in that comparative analysis of control and mutant subclones can be performed in the same tissue environment in vivo. Here, the protocol is described in detail, and experimental paradigms to employ MADM for clonal analysis and lineage tracing in the developing cerebral cortex are demonstrated. Importantly, this protocol can be adapted to perform MADM clonal analysis in any murine stem cell niche, as long as the CreERT2 driver is present.","lang":"eng"}],"oa_version":"Published Version","related_material":{"record":[{"relation":"part_of_dissertation","id":"7902","status":"public"}]},"issue":"159","ec_funded":1,"publication_identifier":{"issn":["1940-087X"]},"publication_status":"published","file":[{"file_id":"7816","checksum":"3154ea7f90b9fb45e084cd1c2770597d","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_name":"jove-protocol-61147-lineage-tracing-clonal-analysis-developing-cerebral-cortex-using.pdf","date_created":"2020-05-11T08:28:38Z","file_size":1352186,"date_updated":"2020-07-14T12:48:03Z","creator":"rbeattie"}],"language":[{"iso":"eng"}],"type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","_id":"7815","department":[{"_id":"SiHi"}],"file_date_updated":"2020-07-14T12:48:03Z","date_updated":"2024-03-27T23:30:41Z","ddc":["570"]},{"project":[{"_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"}],"title":"Genetic dissection of neural development in health and disease at single cell resolution","author":[{"last_name":"Contreras","full_name":"Contreras, Ximena","first_name":"Ximena","id":"475990FE-F248-11E8-B48F-1D18A9856A87"}],"article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Contreras, Ximena. “Genetic Dissection of Neural Development in Health and Disease at Single Cell Resolution.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:7902.","ista":"Contreras X. 2020. Genetic dissection of neural development in health and disease at single cell resolution. Institute of Science and Technology Austria.","mla":"Contreras, Ximena. Genetic Dissection of Neural Development in Health and Disease at Single Cell Resolution. Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:7902.","short":"X. Contreras, Genetic Dissection of Neural Development in Health and Disease at Single Cell Resolution, Institute of Science and Technology Austria, 2020.","ieee":"X. Contreras, “Genetic dissection of neural development in health and disease at single cell resolution,” Institute of Science and Technology Austria, 2020.","apa":"Contreras, X. (2020). Genetic dissection of neural development in health and disease at single cell resolution. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:7902","ama":"Contreras X. Genetic dissection of neural development in health and disease at single cell resolution. 2020. doi:10.15479/AT:ISTA:7902"},"publisher":"Institute of Science and Technology Austria","oa":1,"date_published":"2020-06-05T00:00:00Z","doi":"10.15479/AT:ISTA:7902","date_created":"2020-05-29T08:27:32Z","page":"214","day":"05","has_accepted_license":"1","year":"2020","status":"public","type":"dissertation","_id":"7902","file_date_updated":"2021-06-07T22:30:03Z","department":[{"_id":"SiHi"}],"ddc":["570"],"supervisor":[{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon"}],"date_updated":"2023-10-18T08:45:16Z","month":"06","alternative_title":["ISTA Thesis"],"oa_version":"Published Version","abstract":[{"text":"Mosaic genetic analysis has been widely used in different model organisms such as the fruit fly to study gene-function in a cell-autonomous or tissue-specific fashion. More recently, and less easily conducted, mosaic genetic analysis in mice has also been enabled with the ambition to shed light on human gene function and disease. These genetic tools are of particular interest, but not restricted to, the study of the brain. Notably, the MADM technology offers a genetic approach in mice to visualize and concomitantly manipulate small subsets of genetically defined cells at a clonal level and single cell resolution. MADM-based analysis has already advanced the study of genetic mechanisms regulating brain development and is expected that further MADM-based analysis of genetic alterations will continue to reveal important insights on the fundamental principles of development and disease to potentially assist in the development of new therapies or treatments.\r\nIn summary, this work completed and characterized the necessary genome-wide genetic tools to perform MADM-based analysis at single cell level of the vast majority of mouse genes in virtually any cell type and provided a protocol to perform lineage tracing using the novel MADM resource. Importantly, this work also explored and revealed novel aspects of biologically relevant events in an in vivo context, such as the chromosome-specific bias of chromatid sister segregation pattern, the generation of cell-type diversity in the cerebral cortex and in the cerebellum and finally, the relevance of the interplay between the cell-autonomous gene function and cell-non-autonomous (community) effects in radial glial progenitor lineage progression.\r\nThis work provides a foundation and opens the door to further elucidating the molecular mechanisms underlying neuronal diversity and astrocyte generation.","lang":"eng"}],"acknowledged_ssus":[{"_id":"PreCl"},{"_id":"Bio"}],"related_material":{"record":[{"id":"6830","status":"public","relation":"dissertation_contains"},{"id":"28","status":"public","relation":"dissertation_contains"},{"relation":"dissertation_contains","id":"7815","status":"public"}]},"ec_funded":1,"file":[{"content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","embargo_to":"open_access","access_level":"closed","relation":"source_file","checksum":"43c172bf006c95b65992d473c7240d13","file_id":"7927","date_updated":"2021-06-07T22:30:03Z","file_size":53134142,"creator":"xcontreras","date_created":"2020-06-05T08:18:08Z","file_name":"PhDThesis_Contreras.docx"},{"access_level":"open_access","relation":"main_file","content_type":"application/pdf","checksum":"addfed9128271be05cae3608e03a6ec0","file_id":"7928","embargo":"2021-06-06","creator":"xcontreras","date_updated":"2021-06-07T22:30:03Z","file_size":35117191,"date_created":"2020-06-05T08:18:07Z","file_name":"PhDThesis_Contreras.pdf"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2663-337X"]},"degree_awarded":"PhD","publication_status":"published"},{"file_date_updated":"2020-07-14T12:47:19Z","department":[{"_id":"SiHi"}],"ddc":["570"],"date_updated":"2023-08-24T14:50:50Z","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","_id":"6091","volume":8,"language":[{"iso":"eng"}],"file":[{"relation":"main_file","access_level":"open_access","content_type":"application/pdf","checksum":"7b0800d003f14cd06b1802dea0c52941","file_id":"6098","creator":"dernst","file_size":7260753,"date_updated":"2020-07-14T12:47:19Z","file_name":"2019_eLife_Henderson.pdf","date_created":"2019-03-11T16:15:37Z"}],"publication_status":"published","intvolume":" 8","month":"02","scopus_import":"1","oa_version":"Published Version","pmid":1,"abstract":[{"text":"Cortical networks are characterized by sparse connectivity, with synapses found at only a subset of axo-dendritic contacts. Yet within these networks, neurons can exhibit high connection probabilities, suggesting that cell-intrinsic factors, not proximity, determine connectivity. Here, we identify ephrin-B3 (eB3) as a factor that determines synapse density by mediating a cell-cell competition that requires ephrin-B-EphB signaling. In a microisland culture system designed to isolate cell-cell competition, we find that eB3 determines winning and losing neurons in a contest for synapses. In a Mosaic Analysis with Double Markers (MADM) genetic mouse model system in vivo the relative levels of eB3 control spine density in layer 5 and 6 neurons. MADM cortical neurons in vitro reveal that eB3 controls synapse density independently of action potential-driven activity. Our findings illustrate a new class of competitive mechanism mediated by trans-synaptic organizing proteins which control the number of synapses neurons receive relative to neighboring neurons.","lang":"eng"}],"title":"Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs","article_processing_charge":"No","external_id":{"isi":["000459380600001"],"pmid":["30789343"]},"author":[{"first_name":"Nathan T.","full_name":"Henderson, Nathan T.","last_name":"Henderson"},{"full_name":"Le Marchand, Sylvain J.","last_name":"Le Marchand","first_name":"Sylvain J."},{"full_name":"Hruska, Martin","last_name":"Hruska","first_name":"Martin"},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Liqun","full_name":"Luo, Liqun","last_name":"Luo"},{"full_name":"Dalva, Matthew B.","last_name":"Dalva","first_name":"Matthew B."}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"chicago":"Henderson, Nathan T., Sylvain J. Le Marchand, Martin Hruska, Simon Hippenmeyer, Liqun Luo, and Matthew B. Dalva. “Ephrin-B3 Controls Excitatory Synapse Density through Cell-Cell Competition for EphBs.” ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/eLife.41563.","ista":"Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. 2019. Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs. eLife. 8, e41563.","mla":"Henderson, Nathan T., et al. “Ephrin-B3 Controls Excitatory Synapse Density through Cell-Cell Competition for EphBs.” ELife, vol. 8, e41563, eLife Sciences Publications, 2019, doi:10.7554/eLife.41563.","ama":"Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs. eLife. 2019;8. doi:10.7554/eLife.41563","apa":"Henderson, N. T., Le Marchand, S. J., Hruska, M., Hippenmeyer, S., Luo, L., & Dalva, M. B. (2019). Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.41563","ieee":"N. T. Henderson, S. J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, and M. B. Dalva, “Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs,” eLife, vol. 8. eLife Sciences Publications, 2019.","short":"N.T. Henderson, S.J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, M.B. Dalva, ELife 8 (2019)."},"article_number":"e41563","date_created":"2019-03-10T22:59:20Z","doi":"10.7554/eLife.41563","date_published":"2019-02-21T00:00:00Z","publication":"eLife","day":"21","year":"2019","isi":1,"has_accepted_license":"1","oa":1,"quality_controlled":"1","publisher":"eLife Sciences Publications"},{"ec_funded":1,"issue":"3","volume":235,"language":[{"iso":"eng"}],"file":[{"checksum":"160f960844b204057f20896e0e1f8ee7","file_id":"6845","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2019_JournalAnatomy_Picco.pdf","date_created":"2019-09-02T12:05:18Z","creator":"dernst","file_size":1192994,"date_updated":"2020-07-14T12:47:42Z"}],"publication_status":"published","publication_identifier":{"issn":["0021-8782"],"eissn":["1469-7580"]},"intvolume":" 235","month":"09","scopus_import":"1","oa_version":"Published Version","abstract":[{"lang":"eng","text":"Studying the progression of the proliferative and differentiative patterns of neural stem cells at the individual cell level is crucial to the understanding of cortex development and how the disruption of such patterns can lead to malformations and neurodevelopmental diseases. However, our understanding of the precise lineage progression programme at single-cell resolution is still incomplete due to the technical variations in lineage- tracing approaches. One of the key challenges involves developing a robust theoretical framework in which we can integrate experimental observations and introduce correction factors to obtain a reliable and representative description of the temporal modulation of proliferation and differentiation. In order to obtain more conclusive insights, we carry out virtual clonal analysis using mathematical modelling and compare our results against experimental data. Using a dataset obtained with Mosaic Analysis with Double Markers, we illustrate how the theoretical description can be exploited to interpret and reconcile the disparity between virtual and experimental results."}],"department":[{"_id":"SiHi"}],"file_date_updated":"2020-07-14T12:47:42Z","ddc":["570"],"date_updated":"2023-08-29T07:19:39Z","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc/4.0/legalcode","image":"/images/cc_by_nc.png","name":"Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)","short":"CC BY-NC (4.0)"},"article_type":"original","type":"journal_article","_id":"6844","date_created":"2019-09-02T11:57:28Z","date_published":"2019-09-01T00:00:00Z","doi":"10.1111/joa.13001","page":"686-696","publication":"Journal of Anatomy","day":"01","year":"2019","has_accepted_license":"1","isi":1,"oa":1,"publisher":"Wiley","quality_controlled":"1","title":"A mathematical insight into cell labelling experiments for clonal analysis","external_id":{"isi":["000482426800017"]},"article_processing_charge":"No","author":[{"first_name":"Noemi","last_name":"Picco","full_name":"Picco, Noemi"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"},{"full_name":"Rodarte, Julio","last_name":"Rodarte","first_name":"Julio","id":"3C70A038-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Carmen","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","last_name":"Streicher","full_name":"Streicher, Carmen"},{"first_name":"Zoltán","full_name":"Molnár, Zoltán","last_name":"Molnár"},{"last_name":"Maini","full_name":"Maini, Philip K.","first_name":"Philip K."},{"full_name":"Woolley, Thomas E.","last_name":"Woolley","first_name":"Thomas E."}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ista":"Picco N, Hippenmeyer S, Rodarte J, Streicher C, Molnár Z, Maini PK, Woolley TE. 2019. A mathematical insight into cell labelling experiments for clonal analysis. Journal of Anatomy. 235(3), 686–696.","chicago":"Picco, Noemi, Simon Hippenmeyer, Julio Rodarte, Carmen Streicher, Zoltán Molnár, Philip K. Maini, and Thomas E. Woolley. “A Mathematical Insight into Cell Labelling Experiments for Clonal Analysis.” Journal of Anatomy. Wiley, 2019. https://doi.org/10.1111/joa.13001.","ieee":"N. Picco et al., “A mathematical insight into cell labelling experiments for clonal analysis,” Journal of Anatomy, vol. 235, no. 3. Wiley, pp. 686–696, 2019.","short":"N. Picco, S. Hippenmeyer, J. Rodarte, C. Streicher, Z. Molnár, P.K. Maini, T.E. Woolley, Journal of Anatomy 235 (2019) 686–696.","ama":"Picco N, Hippenmeyer S, Rodarte J, et al. A mathematical insight into cell labelling experiments for clonal analysis. Journal of Anatomy. 2019;235(3):686-696. doi:10.1111/joa.13001","apa":"Picco, N., Hippenmeyer, S., Rodarte, J., Streicher, C., Molnár, Z., Maini, P. K., & Woolley, T. E. (2019). A mathematical insight into cell labelling experiments for clonal analysis. Journal of Anatomy. Wiley. https://doi.org/10.1111/joa.13001","mla":"Picco, Noemi, et al. “A Mathematical Insight into Cell Labelling Experiments for Clonal Analysis.” Journal of Anatomy, vol. 235, no. 3, Wiley, 2019, pp. 686–96, doi:10.1111/joa.13001."},"project":[{"_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780"}]},{"oa":1,"publisher":"Wiley","quality_controlled":"1","year":"2019","isi":1,"has_accepted_license":"1","publication":"Journal of Neurochemistry","day":"01","page":"570-583","date_created":"2019-11-12T14:37:08Z","doi":"10.1111/jnc.14862","date_published":"2019-12-01T00:00:00Z","citation":{"mla":"Cheung, Giselle T., and Michael A. Cousin. “Synaptic Vesicle Generation from Activity‐dependent Bulk Endosomes Requires a Dephosphorylation‐dependent Dynamin–Syndapin Interaction.” Journal of Neurochemistry, vol. 151, no. 5, Wiley, 2019, pp. 570–83, doi:10.1111/jnc.14862.","short":"G.T. Cheung, M.A. Cousin, Journal of Neurochemistry 151 (2019) 570–583.","ieee":"G. T. Cheung and M. A. Cousin, “Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction,” Journal of Neurochemistry, vol. 151, no. 5. Wiley, pp. 570–583, 2019.","apa":"Cheung, G. T., & Cousin, M. A. (2019). Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction. Journal of Neurochemistry. Wiley. https://doi.org/10.1111/jnc.14862","ama":"Cheung GT, Cousin MA. Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction. Journal of Neurochemistry. 2019;151(5):570-583. doi:10.1111/jnc.14862","chicago":"Cheung, Giselle T, and Michael A. Cousin. “Synaptic Vesicle Generation from Activity‐dependent Bulk Endosomes Requires a Dephosphorylation‐dependent Dynamin–Syndapin Interaction.” Journal of Neurochemistry. Wiley, 2019. https://doi.org/10.1111/jnc.14862.","ista":"Cheung GT, Cousin MA. 2019. Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction. Journal of Neurochemistry. 151(5), 570–583."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","external_id":{"isi":["000490703100001"],"pmid":["31479508"]},"article_processing_charge":"No","author":[{"id":"471195F6-F248-11E8-B48F-1D18A9856A87","first_name":"Giselle T","orcid":"0000-0001-8457-2572","full_name":"Cheung, Giselle T","last_name":"Cheung"},{"last_name":"Cousin","full_name":"Cousin, Michael A.","first_name":"Michael A."}],"title":"Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction","abstract":[{"text":"Activity-dependent bulk endocytosis generates synaptic vesicles (SVs) during intense neuronal activity via a two-step process. First, bulk endosomes are formed direct from the plasma membrane from which SVs are then generated. SV generation from bulk endosomes requires the efflux of previously accumulated calcium and activation of the protein phosphatase calcineurin. However, it is still unknown how calcineurin mediates SV generation. We addressed this question using a series of acute interventions that decoupled the generation of SVs from bulk endosomes in rat primary neuronal culture. This was achieved by either disruption of protein–protein interactions via delivery of competitive peptides, or inhibition of enzyme activity by known inhibitors. SV generation was monitored using either a morphological horseradish peroxidase assay or an optical assay that monitors the replenishment of the reserve SV pool. We found that SV generation was inhibited by, (i) peptides that disrupt calcineurin interactions, (ii) an inhibitor of dynamin I GTPase activity and (iii) peptides that disrupt the phosphorylation-dependent dynamin I–syndapin I interaction. Peptides that disrupted syndapin I interactions with eps15 homology domain-containing proteins had no effect. This revealed that (i) calcineurin must be localized at bulk endosomes to mediate its effect, (ii) dynamin I GTPase activity is essential for SV fission and (iii) the calcineurin-dependent interaction between dynamin I and syndapin I is essential for SV generation. We therefore propose that a calcineurin-dependent dephosphorylation cascade that requires both dynamin I GTPase and syndapin I lipid-deforming activity is essential for SV generation from bulk endosomes.","lang":"eng"}],"pmid":1,"oa_version":"Published Version","scopus_import":"1","intvolume":" 151","month":"12","publication_status":"published","publication_identifier":{"issn":["0022-3042"],"eissn":["1471-4159"]},"language":[{"iso":"eng"}],"file":[{"file_id":"7452","checksum":"ec1fb2aebb874009bc309adaada6e1d7","content_type":"application/pdf","access_level":"open_access","relation":"main_file","date_created":"2020-02-05T10:30:02Z","file_name":"2019_JournNeurochemistry_Cheung.pdf","date_updated":"2020-07-14T12:47:47Z","file_size":4334962,"creator":"dernst"}],"volume":151,"issue":"5","_id":"7005","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","status":"public","date_updated":"2023-08-30T07:21:50Z","ddc":["570"],"file_date_updated":"2020-07-14T12:47:47Z","department":[{"_id":"SiHi"}]},{"quality_controlled":"1","publisher":"AAAS","oa":1,"day":"10","publication":"Science","isi":1,"year":"2019","doi":"10.1126/science.aav2522","date_published":"2019-05-10T00:00:00Z","date_created":"2019-05-14T13:07:47Z","article_number":"eaav2522","project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"call_identifier":"FWF","_id":"268F8446-B435-11E9-9278-68D0E5697425","name":"Role of Eed in neural stem cell lineage progression","grant_number":"T0101031"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"mla":"Telley, L., et al. “Temporal Patterning of Apical Progenitors and Their Daughter Neurons in the Developing Neocortex.” Science, vol. 364, no. 6440, eaav2522, AAAS, 2019, doi:10.1126/science.aav2522.","ieee":"L. Telley et al., “Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex,” Science, vol. 364, no. 6440. AAAS, 2019.","short":"L. Telley, G. Agirman, J. Prados, N. Amberg, S. Fièvre, P. Oberst, G. Bartolini, I. Vitali, C. Cadilhac, S. Hippenmeyer, L. Nguyen, A. Dayer, D. Jabaudon, Science 364 (2019).","ama":"Telley L, Agirman G, Prados J, et al. Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex. Science. 2019;364(6440). doi:10.1126/science.aav2522","apa":"Telley, L., Agirman, G., Prados, J., Amberg, N., Fièvre, S., Oberst, P., … Jabaudon, D. (2019). Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex. Science. AAAS. https://doi.org/10.1126/science.aav2522","chicago":"Telley, L, G Agirman, J Prados, Nicole Amberg, S Fièvre, P Oberst, G Bartolini, et al. “Temporal Patterning of Apical Progenitors and Their Daughter Neurons in the Developing Neocortex.” Science. AAAS, 2019. https://doi.org/10.1126/science.aav2522.","ista":"Telley L, Agirman G, Prados J, Amberg N, Fièvre S, Oberst P, Bartolini G, Vitali I, Cadilhac C, Hippenmeyer S, Nguyen L, Dayer A, Jabaudon D. 2019. Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex. Science. 364(6440), eaav2522."},"title":"Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex","author":[{"first_name":"L","full_name":"Telley, L","last_name":"Telley"},{"first_name":"G","last_name":"Agirman","full_name":"Agirman, G"},{"first_name":"J","last_name":"Prados","full_name":"Prados, J"},{"orcid":"0000-0002-3183-8207","full_name":"Amberg, Nicole","last_name":"Amberg","first_name":"Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Fièvre, S","last_name":"Fièvre","first_name":"S"},{"full_name":"Oberst, P","last_name":"Oberst","first_name":"P"},{"first_name":"G","full_name":"Bartolini, G","last_name":"Bartolini"},{"first_name":"I","full_name":"Vitali, I","last_name":"Vitali"},{"last_name":"Cadilhac","full_name":"Cadilhac, C","first_name":"C"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"},{"full_name":"Nguyen, L","last_name":"Nguyen","first_name":"L"},{"full_name":"Dayer, A","last_name":"Dayer","first_name":"A"},{"last_name":"Jabaudon","full_name":"Jabaudon, D","first_name":"D"}],"external_id":{"isi":["000467631800034"],"pmid":["31073041"]},"article_processing_charge":"No","pmid":1,"oa_version":"Published Version","abstract":[{"lang":"eng","text":"During corticogenesis, distinct subtypes of neurons are sequentially born from ventricular zone progenitors. How these cells are molecularly temporally patterned is poorly understood. We used single-cell RNA sequencing at high temporal resolution to trace the lineage of the molecular identities of successive generations of apical progenitors (APs) and their daughter neurons in mouse embryos. We identified a core set of evolutionarily conserved, temporally patterned genes that drive APs from internally driven to more exteroceptive states. We found that the Polycomb repressor complex 2 (PRC2) epigenetically regulates AP temporal progression. Embryonic age–dependent AP molecular states are transmitted to their progeny as successive ground states, onto which essentially conserved early postmitotic differentiation programs are applied, and are complemented by later-occurring environment-dependent signals. Thus, epigenetically regulated temporal molecular birthmarks present in progenitors act in their postmitotic progeny to seed adult neuronal diversity."}],"month":"05","intvolume":" 364","scopus_import":"1","main_file_link":[{"url":"https://orbi.uliege.be/bitstream/2268/239604/1/Telley_Agirman_Science2019.pdf","open_access":"1"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0036-8075"],"eissn":["1095-9203"]},"publication_status":"published","related_material":{"link":[{"description":"News on IST Homepage","url":"https://ist.ac.at/en/news/how-to-generate-a-brain-of-correct-size-and-composition/","relation":"press_release"}]},"volume":364,"issue":"6440","ec_funded":1,"_id":"6455","status":"public","article_type":"original","type":"journal_article","date_updated":"2023-09-05T11:51:09Z","department":[{"_id":"SiHi"}]},{"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"mla":"Ortiz-Álvarez, G., et al. “Adult Neural Stem Cells and Multiciliated Ependymal Cells Share a Common Lineage Regulated by the Geminin Family Members.” Neuron, vol. 102, no. 1, Elsevier, 2019, p. 159–172.e7, doi:10.1016/j.neuron.2019.01.051.","ieee":"G. Ortiz-Álvarez et al., “Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members,” Neuron, vol. 102, no. 1. Elsevier, p. 159–172.e7, 2019.","short":"G. Ortiz-Álvarez, M. Daclin, A. Shihavuddin, P. Lansade, A. Fortoul, M. Faucourt, S. Clavreul, M. Lalioti, S. Taraviras, S. Hippenmeyer, J. Livet, A. Meunier, A. Genovesio, N. Spassky, Neuron 102 (2019) 159–172.e7.","ama":"Ortiz-Álvarez G, Daclin M, Shihavuddin A, et al. Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members. Neuron. 2019;102(1):159-172.e7. doi:10.1016/j.neuron.2019.01.051","apa":"Ortiz-Álvarez, G., Daclin, M., Shihavuddin, A., Lansade, P., Fortoul, A., Faucourt, M., … Spassky, N. (2019). Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2019.01.051","chicago":"Ortiz-Álvarez, G, M Daclin, A Shihavuddin, P Lansade, A Fortoul, M Faucourt, S Clavreul, et al. “Adult Neural Stem Cells and Multiciliated Ependymal Cells Share a Common Lineage Regulated by the Geminin Family Members.” Neuron. Elsevier, 2019. https://doi.org/10.1016/j.neuron.2019.01.051.","ista":"Ortiz-Álvarez G, Daclin M, Shihavuddin A, Lansade P, Fortoul A, Faucourt M, Clavreul S, Lalioti M, Taraviras S, Hippenmeyer S, Livet J, Meunier A, Genovesio A, Spassky N. 2019. Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members. Neuron. 102(1), 159–172.e7."},"title":"Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members","author":[{"last_name":"Ortiz-Álvarez","full_name":"Ortiz-Álvarez, G","first_name":"G"},{"last_name":"Daclin","full_name":"Daclin, M","first_name":"M"},{"full_name":"Shihavuddin, A","last_name":"Shihavuddin","first_name":"A"},{"first_name":"P","full_name":"Lansade, P","last_name":"Lansade"},{"full_name":"Fortoul, A","last_name":"Fortoul","first_name":"A"},{"first_name":"M","full_name":"Faucourt, M","last_name":"Faucourt"},{"full_name":"Clavreul, S","last_name":"Clavreul","first_name":"S"},{"first_name":"ME","full_name":"Lalioti, ME","last_name":"Lalioti"},{"last_name":"Taraviras","full_name":"Taraviras, S","first_name":"S"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon"},{"last_name":"Livet","full_name":"Livet, J","first_name":"J"},{"last_name":"Meunier","full_name":"Meunier, A","first_name":"A"},{"last_name":"Genovesio","full_name":"Genovesio, A","first_name":"A"},{"first_name":"N","full_name":"Spassky, N","last_name":"Spassky"}],"external_id":{"pmid":["30824354"],"isi":["000463337900018"]},"article_processing_charge":"No","project":[{"grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425"}],"day":"03","publication":"Neuron","has_accepted_license":"1","isi":1,"year":"2019","doi":"10.1016/j.neuron.2019.01.051","date_published":"2019-04-03T00:00:00Z","date_created":"2019-05-14T13:06:30Z","page":"159-172.e7","quality_controlled":"1","publisher":"Elsevier","oa":1,"ddc":["570"],"date_updated":"2023-09-05T13:02:21Z","file_date_updated":"2020-07-14T12:47:30Z","department":[{"_id":"SiHi"}],"_id":"6454","status":"public","type":"journal_article","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"file":[{"file_id":"6457","checksum":"1fb6e195c583eb0c5cabf26f69ff6675","access_level":"open_access","relation":"main_file","content_type":"application/pdf","date_created":"2019-05-15T09:28:41Z","file_name":"2019_Neuron_Ortiz.pdf","creator":"dernst","date_updated":"2020-07-14T12:47:30Z","file_size":7288572}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0896-6273"],"eissn":["1097-4199"]},"publication_status":"published","issue":"1","volume":102,"ec_funded":1,"oa_version":"Published Version","pmid":1,"abstract":[{"text":"Adult neural stem cells and multiciliated ependymalcells are glial cells essential for neurological func-tions. Together, they make up the adult neurogenicniche. Using both high-throughput clonal analysisand single-cell resolution of progenitor division pat-terns and fate, we show that these two componentsof the neurogenic niche are lineally related: adult neu-ral stem cells are sister cells to ependymal cells,whereas most ependymal cells arise from the termi-nal symmetric divisions of the lineage. Unexpectedly,we found that the antagonist regulators of DNA repli-cation, GemC1 and Geminin, can tune the proportionof neural stem cells and ependymal cells. Our find-ings reveal the controlled dynamic of the neurogenicniche ontogeny and identify the Geminin familymembers as key regulators of the initial pool of adultneural stem cells.","lang":"eng"}],"month":"04","intvolume":" 102","scopus_import":"1"},{"citation":{"ama":"Llorca A, Ciceri G, Beattie RJ, et al. A stochastic framework of neurogenesis underlies the assembly of neocortical cytoarchitecture. eLife. 2019;8. doi:10.7554/eLife.51381","apa":"Llorca, A., Ciceri, G., Beattie, R. J., Wong, F. K., Diana, G., Serafeimidou-Pouliou, E., … Marín, O. (2019). A stochastic framework of neurogenesis underlies the assembly of neocortical cytoarchitecture. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.51381","short":"A. Llorca, G. Ciceri, R.J. Beattie, F.K. Wong, G. Diana, E. Serafeimidou-Pouliou, M. Fernández-Otero, C. Streicher, S.J. Arnold, M. Meyer, S. Hippenmeyer, M. Maravall, O. Marín, ELife 8 (2019).","ieee":"A. Llorca et al., “A stochastic framework of neurogenesis underlies the assembly of neocortical cytoarchitecture,” eLife, vol. 8. eLife Sciences Publications, 2019.","mla":"Llorca, Alfredo, et al. “A Stochastic Framework of Neurogenesis Underlies the Assembly of Neocortical Cytoarchitecture.” ELife, vol. 8, e51381, eLife Sciences Publications, 2019, doi:10.7554/eLife.51381.","ista":"Llorca A, Ciceri G, Beattie RJ, Wong FK, Diana G, Serafeimidou-Pouliou E, Fernández-Otero M, Streicher C, Arnold SJ, Meyer M, Hippenmeyer S, Maravall M, Marín O. 2019. A stochastic framework of neurogenesis underlies the assembly of neocortical cytoarchitecture. eLife. 8, e51381.","chicago":"Llorca, Alfredo, Gabriele Ciceri, Robert J Beattie, Fong Kuan Wong, Giovanni Diana, Eleni Serafeimidou-Pouliou, Marian Fernández-Otero, et al. “A Stochastic Framework of Neurogenesis Underlies the Assembly of Neocortical Cytoarchitecture.” ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/eLife.51381."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","external_id":{"pmid":["31736464"],"isi":["000508156800001"]},"article_processing_charge":"No","author":[{"first_name":"Alfredo","full_name":"Llorca, Alfredo","last_name":"Llorca"},{"first_name":"Gabriele","last_name":"Ciceri","full_name":"Ciceri, Gabriele"},{"id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","first_name":"Robert J","orcid":"0000-0002-8483-8753","full_name":"Beattie, Robert J","last_name":"Beattie"},{"last_name":"Wong","full_name":"Wong, Fong Kuan","first_name":"Fong Kuan"},{"full_name":"Diana, Giovanni","last_name":"Diana","first_name":"Giovanni"},{"last_name":"Serafeimidou-Pouliou","full_name":"Serafeimidou-Pouliou, Eleni","first_name":"Eleni"},{"full_name":"Fernández-Otero, Marian","last_name":"Fernández-Otero","first_name":"Marian"},{"id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","first_name":"Carmen","full_name":"Streicher, Carmen","last_name":"Streicher"},{"last_name":"Arnold","full_name":"Arnold, Sebastian J.","first_name":"Sebastian J."},{"first_name":"Martin","full_name":"Meyer, Martin","last_name":"Meyer"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061"},{"first_name":"Miguel","full_name":"Maravall, Miguel","last_name":"Maravall"},{"first_name":"Oscar","last_name":"Marín","full_name":"Marín, Oscar"}],"title":"A stochastic framework of neurogenesis underlies the assembly of neocortical cytoarchitecture","article_number":"e51381","project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"grant_number":"M02416","name":"Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex","_id":"264E56E2-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"year":"2019","isi":1,"has_accepted_license":"1","publication":"eLife","day":"18","date_created":"2019-12-22T23:00:42Z","doi":"10.7554/eLife.51381","date_published":"2019-11-18T00:00:00Z","oa":1,"quality_controlled":"1","publisher":"eLife Sciences Publications","date_updated":"2023-09-06T14:38:39Z","ddc":["570"],"file_date_updated":"2020-07-14T12:47:53Z","department":[{"_id":"SiHi"}],"_id":"7202","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"original","type":"journal_article","status":"public","publication_status":"published","publication_identifier":{"eissn":["2050084X"]},"language":[{"iso":"eng"}],"file":[{"file_name":"2019_eLife_Llorca.pdf","date_created":"2020-02-18T15:19:26Z","file_size":2960543,"date_updated":"2020-07-14T12:47:53Z","creator":"dernst","checksum":"b460ecc33e1a68265e7adea775021f3a","file_id":"7503","content_type":"application/pdf","relation":"main_file","access_level":"open_access"}],"ec_funded":1,"volume":8,"abstract":[{"lang":"eng","text":"The cerebral cortex contains multiple areas with distinctive cytoarchitectonical patterns, but the cellular mechanisms underlying the emergence of this diversity remain unclear. Here, we have investigated the neuronal output of individual progenitor cells in the developing mouse neocortex using a combination of methods that together circumvent the biases and limitations of individual approaches. Our experimental results indicate that progenitor cells generate pyramidal cell lineages with a wide range of sizes and laminar configurations. Mathematical modelling indicates that these outcomes are compatible with a stochastic model of cortical neurogenesis in which progenitor cells undergo a series of probabilistic decisions that lead to the specification of very heterogeneous progenies. Our findings support a mechanism for cortical neurogenesis whose flexibility would make it capable to generate the diverse cytoarchitectures that characterize distinct neocortical areas."}],"oa_version":"Published Version","pmid":1,"scopus_import":"1","intvolume":" 8","month":"11"},{"date_updated":"2023-09-08T11:38:04Z","ddc":["570"],"department":[{"_id":"SiHi"}],"file_date_updated":"2020-07-14T12:47:30Z","_id":"6451","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"type":"journal_article","status":"public","publication_status":"published","publication_identifier":{"issn":["2589-0042"]},"language":[{"iso":"eng"}],"file":[{"creator":"dernst","file_size":8365970,"date_updated":"2020-07-14T12:47:30Z","file_name":"2019_iScience_Amberg.pdf","date_created":"2019-05-14T11:51:51Z","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_id":"6452","checksum":"a9ad2296726c9474ad5860c9c2f53622"}],"volume":15,"abstract":[{"text":"Epidermal growth factor receptor (EGFR) signaling controls skin development and homeostasis inmice and humans, and its deficiency causes severe skin inflammation, which might affect epidermalstem cell behavior. Here, we describe the inflammation-independent effects of EGFR deficiency dur-ing skin morphogenesis and in adult hair follicle stem cells. Expression and alternative splicing analysisof RNA sequencing data from interfollicular epidermis and outer root sheath indicate that EGFR con-trols genes involved in epidermal differentiation and also in centrosome function, DNA damage, cellcycle, and apoptosis. Genetic experiments employingp53deletion in EGFR-deficient epidermis revealthat EGFR signaling exhibitsp53-dependent functions in proliferative epidermal compartments, aswell asp53-independent functions in differentiated hair shaft keratinocytes. Loss of EGFR leads toabsence of LEF1 protein specifically in the innermost epithelial hair layers, resulting in disorganizationof medulla cells. Thus, our results uncover important spatial and temporal features of cell-autonomousEGFR functions in the epidermis.","lang":"eng"}],"oa_version":"Published Version","intvolume":" 15","month":"05","citation":{"ista":"Amberg N, Sotiropoulou PA, Heller G, Lichtenberger BM, Holcmann M, Camurdanoglu B, Baykuscheva-Gentscheva T, Blanpain C, Sibilia M. 2019. EGFR controls hair shaft differentiation in a p53-independent manner. iScience. 15, 243–256.","chicago":"Amberg, Nicole, Panagiota A. Sotiropoulou, Gerwin Heller, Beate M. Lichtenberger, Martin Holcmann, Bahar Camurdanoglu, Temenuschka Baykuscheva-Gentscheva, Cedric Blanpain, and Maria Sibilia. “EGFR Controls Hair Shaft Differentiation in a P53-Independent Manner.” IScience. Elsevier, 2019. https://doi.org/10.1016/j.isci.2019.04.018.","ieee":"N. Amberg et al., “EGFR controls hair shaft differentiation in a p53-independent manner,” iScience, vol. 15. Elsevier, pp. 243–256, 2019.","short":"N. Amberg, P.A. Sotiropoulou, G. Heller, B.M. Lichtenberger, M. Holcmann, B. Camurdanoglu, T. Baykuscheva-Gentscheva, C. Blanpain, M. Sibilia, IScience 15 (2019) 243–256.","apa":"Amberg, N., Sotiropoulou, P. A., Heller, G., Lichtenberger, B. M., Holcmann, M., Camurdanoglu, B., … Sibilia, M. (2019). EGFR controls hair shaft differentiation in a p53-independent manner. IScience. Elsevier. https://doi.org/10.1016/j.isci.2019.04.018","ama":"Amberg N, Sotiropoulou PA, Heller G, et al. EGFR controls hair shaft differentiation in a p53-independent manner. iScience. 2019;15:243-256. doi:10.1016/j.isci.2019.04.018","mla":"Amberg, Nicole, et al. “EGFR Controls Hair Shaft Differentiation in a P53-Independent Manner.” IScience, vol. 15, Elsevier, 2019, pp. 243–56, doi:10.1016/j.isci.2019.04.018."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","external_id":{"isi":["000470104600022"]},"article_processing_charge":"No","author":[{"full_name":"Amberg, Nicole","orcid":"0000-0002-3183-8207","last_name":"Amberg","first_name":"Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Sotiropoulou, Panagiota A.","last_name":"Sotiropoulou","first_name":"Panagiota A."},{"last_name":"Heller","full_name":"Heller, Gerwin","first_name":"Gerwin"},{"first_name":"Beate M.","full_name":"Lichtenberger, Beate M.","last_name":"Lichtenberger"},{"last_name":"Holcmann","full_name":"Holcmann, Martin","first_name":"Martin"},{"full_name":"Camurdanoglu, Bahar","last_name":"Camurdanoglu","first_name":"Bahar"},{"last_name":"Baykuscheva-Gentscheva","full_name":"Baykuscheva-Gentscheva, Temenuschka","first_name":"Temenuschka"},{"last_name":"Blanpain","full_name":"Blanpain, Cedric","first_name":"Cedric"},{"last_name":"Sibilia","full_name":"Sibilia, Maria","first_name":"Maria"}],"title":"EGFR controls hair shaft differentiation in a p53-independent manner","year":"2019","isi":1,"has_accepted_license":"1","publication":"iScience","day":"31","page":"243-256","date_created":"2019-05-14T11:47:40Z","doi":"10.1016/j.isci.2019.04.018","date_published":"2019-05-31T00:00:00Z","oa":1,"quality_controlled":"1","publisher":"Elsevier"},{"project":[{"grant_number":"LS13-002","name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain","_id":"25D92700-B435-11E9-9278-68D0E5697425"},{"grant_number":"RGP0053/2014","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level","_id":"25D7962E-B435-11E9-9278-68D0E5697425"},{"_id":"25D61E48-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Molecular Mechanisms of Cerebral Cortex Development","grant_number":"618444"},{"grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"ama":"Amberg N, Laukoter S, Hippenmeyer S. Epigenetic cues modulating the generation of cell type diversity in the cerebral cortex. Journal of Neurochemistry. 2019;149(1):12-26. doi:10.1111/jnc.14601","apa":"Amberg, N., Laukoter, S., & Hippenmeyer, S. (2019). Epigenetic cues modulating the generation of cell type diversity in the cerebral cortex. Journal of Neurochemistry. Wiley. https://doi.org/10.1111/jnc.14601","short":"N. Amberg, S. Laukoter, S. Hippenmeyer, Journal of Neurochemistry 149 (2019) 12–26.","ieee":"N. Amberg, S. Laukoter, and S. Hippenmeyer, “Epigenetic cues modulating the generation of cell type diversity in the cerebral cortex,” Journal of Neurochemistry, vol. 149, no. 1. Wiley, pp. 12–26, 2019.","mla":"Amberg, Nicole, et al. “Epigenetic Cues Modulating the Generation of Cell Type Diversity in the Cerebral Cortex.” Journal of Neurochemistry, vol. 149, no. 1, Wiley, 2019, pp. 12–26, doi:10.1111/jnc.14601.","ista":"Amberg N, Laukoter S, Hippenmeyer S. 2019. Epigenetic cues modulating the generation of cell type diversity in the cerebral cortex. Journal of Neurochemistry. 149(1), 12–26.","chicago":"Amberg, Nicole, Susanne Laukoter, and Simon Hippenmeyer. “Epigenetic Cues Modulating the Generation of Cell Type Diversity in the Cerebral Cortex.” Journal of Neurochemistry. Wiley, 2019. https://doi.org/10.1111/jnc.14601."},"title":"Epigenetic cues modulating the generation of cell type diversity in the cerebral cortex","external_id":{"isi":["000462680200002"]},"article_processing_charge":"Yes (via OA deal)","author":[{"last_name":"Amberg","full_name":"Amberg, Nicole","orcid":"0000-0002-3183-8207","first_name":"Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Susanne","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7903-3010","full_name":"Laukoter, Susanne","last_name":"Laukoter"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer"}],"acknowledgement":" This work was supported by IST Austria institutional funds; NÖ Forschung und Bildung \r\nn[f+b] (C13-002) to SH; a program grant from the Human Frontiers Science Program (RGP0053/2014) to SH; the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement No 618444 to SH, and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement No 725780 LinPro)to SH.\r\n","oa":1,"publisher":"Wiley","quality_controlled":"1","publication":"Journal of Neurochemistry","day":"01","year":"2019","has_accepted_license":"1","isi":1,"date_created":"2018-12-11T11:44:14Z","doi":"10.1111/jnc.14601","date_published":"2019-04-01T00:00:00Z","page":"12-26","_id":"27","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"review","ddc":["570"],"date_updated":"2023-09-11T13:40:26Z","department":[{"_id":"SiHi"}],"file_date_updated":"2020-07-14T12:45:45Z","oa_version":"Published Version","abstract":[{"text":"The cerebral cortex is composed of a large variety of distinct cell-types including projection neurons, interneurons and glial cells which emerge from distinct neural stem cell (NSC) lineages. The vast majority of cortical projection neurons and certain classes of glial cells are generated by radial glial progenitor cells (RGPs) in a highly orchestrated manner. Recent studies employing single cell analysis and clonal lineage tracing suggest that NSC and RGP lineage progression are regulated in a profound deterministic manner. In this review we focus on recent advances based mainly on correlative phenotypic data emerging from functional genetic studies in mice. We establish hypotheses to test in future research and outline a conceptual framework how epigenetic cues modulate the generation of cell-type diversity during cortical development. This article is protected by copyright. All rights reserved.","lang":"eng"}],"intvolume":" 149","month":"04","scopus_import":"1","language":[{"iso":"eng"}],"file":[{"date_created":"2020-01-07T13:35:52Z","file_name":"2019_Wiley_Amberg.pdf","creator":"kschuh","date_updated":"2020-07-14T12:45:45Z","file_size":889709,"checksum":"db027721a95d36f5de36aadcd0bdf7e6","file_id":"7239","access_level":"open_access","relation":"main_file","content_type":"application/pdf"}],"publication_status":"published","ec_funded":1,"volume":149,"issue":"1"},{"quality_controlled":"1","publisher":"Public Library of Science","oa":1,"date_published":"2019-07-22T00:00:00Z","doi":"10.1371/journal.pgen.1008268","date_created":"2020-01-29T16:14:07Z","day":"22","publication":"PLoS Genetics","isi":1,"has_accepted_license":"1","year":"2019","article_number":"e1008268","title":"The Airn lncRNA does not require any DNA elements within its locus to silence distant imprinted genes","author":[{"first_name":"Daniel","full_name":"Andergassen, Daniel","last_name":"Andergassen"},{"full_name":"Muckenhuber, Markus","last_name":"Muckenhuber","first_name":"Markus"},{"first_name":"Philipp C.","full_name":"Bammer, Philipp C.","last_name":"Bammer"},{"full_name":"Kulinski, Tomasz M.","last_name":"Kulinski","first_name":"Tomasz M."},{"full_name":"Theussl, Hans-Christian","last_name":"Theussl","first_name":"Hans-Christian"},{"first_name":"Takahiko","last_name":"Shimizu","full_name":"Shimizu, Takahiko"},{"last_name":"Penninger","full_name":"Penninger, Josef M.","first_name":"Josef M."},{"full_name":"Pauler, Florian","orcid":"0000-0002-7462-0048","last_name":"Pauler","first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Quanah J.","full_name":"Hudson, Quanah J.","last_name":"Hudson"}],"external_id":{"isi":["000478689100025"],"pmid":["31329595"]},"article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"short":"D. Andergassen, M. Muckenhuber, P.C. Bammer, T.M. Kulinski, H.-C. Theussl, T. Shimizu, J.M. Penninger, F. Pauler, Q.J. Hudson, PLoS Genetics 15 (2019).","ieee":"D. Andergassen et al., “The Airn lncRNA does not require any DNA elements within its locus to silence distant imprinted genes,” PLoS Genetics, vol. 15, no. 7. Public Library of Science, 2019.","ama":"Andergassen D, Muckenhuber M, Bammer PC, et al. The Airn lncRNA does not require any DNA elements within its locus to silence distant imprinted genes. PLoS Genetics. 2019;15(7). doi:10.1371/journal.pgen.1008268","apa":"Andergassen, D., Muckenhuber, M., Bammer, P. C., Kulinski, T. M., Theussl, H.-C., Shimizu, T., … Hudson, Q. J. (2019). The Airn lncRNA does not require any DNA elements within its locus to silence distant imprinted genes. PLoS Genetics. Public Library of Science. https://doi.org/10.1371/journal.pgen.1008268","mla":"Andergassen, Daniel, et al. “The Airn LncRNA Does Not Require Any DNA Elements within Its Locus to Silence Distant Imprinted Genes.” PLoS Genetics, vol. 15, no. 7, e1008268, Public Library of Science, 2019, doi:10.1371/journal.pgen.1008268.","ista":"Andergassen D, Muckenhuber M, Bammer PC, Kulinski TM, Theussl H-C, Shimizu T, Penninger JM, Pauler F, Hudson QJ. 2019. The Airn lncRNA does not require any DNA elements within its locus to silence distant imprinted genes. PLoS Genetics. 15(7), e1008268.","chicago":"Andergassen, Daniel, Markus Muckenhuber, Philipp C. Bammer, Tomasz M. Kulinski, Hans-Christian Theussl, Takahiko Shimizu, Josef M. Penninger, Florian Pauler, and Quanah J. Hudson. “The Airn LncRNA Does Not Require Any DNA Elements within Its Locus to Silence Distant Imprinted Genes.” PLoS Genetics. Public Library of Science, 2019. https://doi.org/10.1371/journal.pgen.1008268."},"month":"07","intvolume":" 15","scopus_import":"1","oa_version":"Published Version","pmid":1,"abstract":[{"text":"Long non-coding (lnc) RNAs are numerous and found throughout the mammalian genome, and many are thought to be involved in the regulation of gene expression. However, the majority remain relatively uncharacterised and of uncertain function making the use of model systems to uncover their mode of action valuable. Imprinted lncRNAs target and recruit epigenetic silencing factors to a cluster of imprinted genes on the same chromosome, making them one of the best characterized lncRNAs for silencing distant genes in cis. In this study we examined silencing of the distant imprinted gene Slc22a3 by the lncRNA Airn in the Igf2r imprinted cluster in mouse. Previously we proposed that imprinted lncRNAs may silence distant imprinted genes by disrupting promoter-enhancer interactions by being transcribed through the enhancer, which we called the enhancer interference hypothesis. Here we tested this hypothesis by first using allele-specific chromosome conformation capture (3C) to detect interactions between the Slc22a3 promoter and the locus of the Airn lncRNA that silences it on the paternal chromosome. In agreement with the model, we found interactions enriched on the maternal allele across the entire Airn gene consistent with multiple enhancer-promoter interactions. Therefore, to test the enhancer interference hypothesis we devised an approach to delete the entire Airn gene. However, the deletion showed that there are no essential enhancers for Slc22a2, Pde10a and Slc22a3 within the Airn gene, strongly indicating that the Airn RNA rather than its transcription is responsible for silencing distant imprinted genes. Furthermore, we found that silent imprinted genes were covered with large blocks of H3K27me3 on the repressed paternal allele. Therefore we propose an alternative hypothesis whereby the chromosome interactions may initially guide the lncRNA to target imprinted promoters and recruit repressive chromatin, and that these interactions are lost once silencing is established.","lang":"eng"}],"issue":"7","volume":15,"file":[{"date_created":"2020-02-04T10:11:55Z","file_name":"2019_PlosGenetics_Andergassen.pdf","date_updated":"2020-07-14T12:47:57Z","file_size":2302307,"creator":"dernst","checksum":"2f51fc91e4a4199827adc51d432ad864","file_id":"7446","content_type":"application/pdf","access_level":"open_access","relation":"main_file"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["1553-7404"]},"publication_status":"published","status":"public","type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"7399","department":[{"_id":"SiHi"}],"file_date_updated":"2020-07-14T12:47:57Z","ddc":["570"],"date_updated":"2023-10-17T12:30:27Z"},{"intvolume":" 103","month":"09","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.neuron.2019.08.021"}],"scopus_import":"1","oa_version":"Published Version","pmid":1,"related_material":{"record":[{"id":"7902","status":"public","relation":"part_of_dissertation"}]},"issue":"5","volume":103,"language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"issn":["08966273"],"eissn":["10974199"]},"status":"public","type":"journal_article","article_type":"letter_note","_id":"6830","department":[{"_id":"SiHi"}],"date_updated":"2024-03-27T23:30:41Z","oa":1,"publisher":"Elsevier","quality_controlled":"1","date_created":"2019-08-25T22:00:50Z","date_published":"2019-09-04T00:00:00Z","doi":"10.1016/j.neuron.2019.08.021","page":"750-752","publication":"Neuron","day":"04","year":"2019","isi":1,"title":"Memo1 tiles the radial glial cell grid","article_processing_charge":"No","external_id":{"isi":["000484400200002"],"pmid":["31487522"]},"author":[{"id":"475990FE-F248-11E8-B48F-1D18A9856A87","first_name":"Ximena","last_name":"Contreras","full_name":"Contreras, Ximena"},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ama":"Contreras X, Hippenmeyer S. Memo1 tiles the radial glial cell grid. Neuron. 2019;103(5):750-752. doi:10.1016/j.neuron.2019.08.021","apa":"Contreras, X., & Hippenmeyer, S. (2019). Memo1 tiles the radial glial cell grid. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2019.08.021","ieee":"X. Contreras and S. Hippenmeyer, “Memo1 tiles the radial glial cell grid,” Neuron, vol. 103, no. 5. Elsevier, pp. 750–752, 2019.","short":"X. Contreras, S. Hippenmeyer, Neuron 103 (2019) 750–752.","mla":"Contreras, Ximena, and Simon Hippenmeyer. “Memo1 Tiles the Radial Glial Cell Grid.” Neuron, vol. 103, no. 5, Elsevier, 2019, pp. 750–52, doi:10.1016/j.neuron.2019.08.021.","ista":"Contreras X, Hippenmeyer S. 2019. Memo1 tiles the radial glial cell grid. Neuron. 103(5), 750–752.","chicago":"Contreras, Ximena, and Simon Hippenmeyer. “Memo1 Tiles the Radial Glial Cell Grid.” Neuron. Elsevier, 2019. https://doi.org/10.1016/j.neuron.2019.08.021."}},{"type":"preprint","status":"public","project":[{"call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780"},{"name":"Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex","grant_number":"M02416","call_identifier":"FWF","_id":"264E56E2-B435-11E9-9278-68D0E5697425"}],"_id":"8547","article_processing_charge":"No","author":[{"full_name":"Llorca, Alfredo","last_name":"Llorca","first_name":"Alfredo"},{"last_name":"Ciceri","full_name":"Ciceri, Gabriele","first_name":"Gabriele"},{"id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","first_name":"Robert J","last_name":"Beattie","orcid":"0000-0002-8483-8753","full_name":"Beattie, Robert J"},{"full_name":"Wong, Fong K.","last_name":"Wong","first_name":"Fong K."},{"first_name":"Giovanni","last_name":"Diana","full_name":"Diana, Giovanni"},{"first_name":"Eleni","full_name":"Serafeimidou, Eleni","last_name":"Serafeimidou"},{"last_name":"Fernández-Otero","full_name":"Fernández-Otero, Marian","first_name":"Marian"},{"full_name":"Streicher, Carmen","last_name":"Streicher","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","first_name":"Carmen"},{"full_name":"Arnold, Sebastian J.","last_name":"Arnold","first_name":"Sebastian J."},{"last_name":"Meyer","full_name":"Meyer, Martin","first_name":"Martin"},{"orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"},{"last_name":"Maravall","full_name":"Maravall, Miguel","first_name":"Miguel"},{"last_name":"Marín","full_name":"Marín, Oscar","first_name":"Oscar"}],"title":"Heterogeneous progenitor cell behaviors underlie the assembly of neocortical cytoarchitecture","department":[{"_id":"SiHi"}],"citation":{"mla":"Llorca, Alfredo, et al. “Heterogeneous Progenitor Cell Behaviors Underlie the Assembly of Neocortical Cytoarchitecture.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/494088.","ama":"Llorca A, Ciceri G, Beattie RJ, et al. Heterogeneous progenitor cell behaviors underlie the assembly of neocortical cytoarchitecture. bioRxiv. doi:10.1101/494088","apa":"Llorca, A., Ciceri, G., Beattie, R. J., Wong, F. K., Diana, G., Serafeimidou, E., … Marín, O. (n.d.). Heterogeneous progenitor cell behaviors underlie the assembly of neocortical cytoarchitecture. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/494088","short":"A. Llorca, G. Ciceri, R.J. Beattie, F.K. Wong, G. Diana, E. Serafeimidou, M. Fernández-Otero, C. Streicher, S.J. Arnold, M. Meyer, S. Hippenmeyer, M. Maravall, O. Marín, BioRxiv (n.d.).","ieee":"A. Llorca et al., “Heterogeneous progenitor cell behaviors underlie the assembly of neocortical cytoarchitecture,” bioRxiv. Cold Spring Harbor Laboratory.","chicago":"Llorca, Alfredo, Gabriele Ciceri, Robert J Beattie, Fong K. Wong, Giovanni Diana, Eleni Serafeimidou, Marian Fernández-Otero, et al. “Heterogeneous Progenitor Cell Behaviors Underlie the Assembly of Neocortical Cytoarchitecture.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/494088.","ista":"Llorca A, Ciceri G, Beattie RJ, Wong FK, Diana G, Serafeimidou E, Fernández-Otero M, Streicher C, Arnold SJ, Meyer M, Hippenmeyer S, Maravall M, Marín O. Heterogeneous progenitor cell behaviors underlie the assembly of neocortical cytoarchitecture. bioRxiv, 10.1101/494088."},"date_updated":"2021-01-12T08:20:00Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/494088"}],"oa":1,"publisher":"Cold Spring Harbor Laboratory","month":"12","abstract":[{"lang":"eng","text":"The cerebral cortex contains multiple hierarchically organized areas with distinctive cytoarchitectonical patterns, but the cellular mechanisms underlying the emergence of this diversity remain unclear. Here, we have quantitatively investigated the neuronal output of individual progenitor cells in the ventricular zone of the developing mouse neocortex using a combination of methods that together circumvent the biases and limitations of individual approaches. We found that individual cortical progenitor cells show a high degree of stochasticity and generate pyramidal cell lineages that adopt a wide range of laminar configurations. Mathematical modelling these lineage data suggests that a small number of progenitor cell populations, each generating pyramidal cells following different stochastic developmental programs, suffice to generate the heterogenous complement of pyramidal cell lineages that collectively build the complex cytoarchitecture of the neocortex."}],"acknowledgement":"We thank I. Andrew and S.E. Bae for excellent technical assistance, F. Gage for plasmids, and K. Nave (Nex-Cre) for mouse colonies. We thank members of the Marín and Rico laboratories for stimulating discussions and ideas. Our research on this topic is supported by grants from the European Research Council (ERC-2017-AdG 787355 to O.M and ERC2016-CoG 725780 to S.H.) and Wellcome Trust (103714MA) to O.M. L.L. was the recipient of an EMBO long-term postdoctoral fellowship, R.B. received support from FWF Lise-Meitner program (M 2416) and F.K.W. was supported by an EMBO postdoctoral fellowship and is currently a Marie Skłodowska-Curie Fellow from the European Commission under the H2020 Programme.","oa_version":"Preprint","date_created":"2020-09-21T12:01:50Z","ec_funded":1,"doi":"10.1101/494088","date_published":"2018-12-13T00:00:00Z","publication_status":"submitted","year":"2018","language":[{"iso":"eng"}],"publication":"bioRxiv","day":"13"},{"publication_identifier":{"issn":["1471-2164"]},"publication_status":"published","file":[{"checksum":"a56516e734dab589dc7f3e1915973b4d","file_id":"5712","content_type":"application/pdf","access_level":"open_access","relation":"main_file","date_created":"2018-12-17T14:52:57Z","file_name":"2018_BMCGenomics_Higareda.pdf","date_updated":"2020-07-14T12:45:23Z","file_size":4629784,"creator":"dernst"}],"language":[{"iso":"eng"}],"volume":19,"issue":"1","related_material":{"record":[{"relation":"research_data","id":"9807","status":"public"},{"id":"9808","status":"public","relation":"research_data"}]},"abstract":[{"lang":"eng","text":"Background: Norepinephrine (NE) signaling has a key role in white adipose tissue (WAT) functions, including lipolysis, free fatty acid liberation and, under certain conditions, conversion of white into brite (brown-in-white) adipocytes. However, acute effects of NE stimulation have not been described at the transcriptional network level. Results: We used RNA-seq to uncover a broad transcriptional response. The inference of protein-protein and protein-DNA interaction networks allowed us to identify a set of immediate-early genes (IEGs) with high betweenness, validating our approach and suggesting a hierarchical control of transcriptional regulation. In addition, we identified a transcriptional regulatory network with IEGs as master regulators, including HSF1 and NFIL3 as novel NE-induced IEG candidates. Moreover, a functional enrichment analysis and gene clustering into functional modules suggest a crosstalk between metabolic, signaling, and immune responses. Conclusions: Altogether, our network biology approach explores for the first time the immediate-early systems level response of human adipocytes to acute sympathetic activation, thereby providing a first network basis of early cell fate programs and crosstalks between metabolic and transcriptional networks required for proper WAT function."}],"oa_version":"Published Version","scopus_import":"1","month":"11","intvolume":" 19","date_updated":"2023-09-13T09:10:47Z","ddc":["570"],"department":[{"_id":"SiHi"}],"file_date_updated":"2020-07-14T12:45:23Z","_id":"20","article_type":"original","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","isi":1,"has_accepted_license":"1","year":"2018","day":"03","publication":"BMC Genomics","doi":"10.1186/s12864-018-5173-0","date_published":"2018-11-03T00:00:00Z","date_created":"2018-12-11T11:44:12Z","acknowledgement":"This work was funded by the German Centre for Diabetes Research (DZD) and the Austrian Science Fund (FWF, P25729-B19).","quality_controlled":"1","publisher":"BioMed Central","oa":1,"citation":{"ista":"Higareda Almaraz J, Karbiener M, Giroud M, Pauler F, Gerhalter T, Herzig S, Scheideler M. 2018. Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. BMC Genomics. 19(1).","chicago":"Higareda Almaraz, Juan, Michael Karbiener, Maude Giroud, Florian Pauler, Teresa Gerhalter, Stephan Herzig, and Marcel Scheideler. “Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes.” BMC Genomics. BioMed Central, 2018. https://doi.org/10.1186/s12864-018-5173-0.","ieee":"J. Higareda Almaraz et al., “Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes,” BMC Genomics, vol. 19, no. 1. BioMed Central, 2018.","short":"J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S. Herzig, M. Scheideler, BMC Genomics 19 (2018).","apa":"Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T., Herzig, S., & Scheideler, M. (2018). Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. BMC Genomics. BioMed Central. https://doi.org/10.1186/s12864-018-5173-0","ama":"Higareda Almaraz J, Karbiener M, Giroud M, et al. Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. BMC Genomics. 2018;19(1). doi:10.1186/s12864-018-5173-0","mla":"Higareda Almaraz, Juan, et al. “Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes.” BMC Genomics, vol. 19, no. 1, BioMed Central, 2018, doi:10.1186/s12864-018-5173-0."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","author":[{"full_name":"Higareda Almaraz, Juan","last_name":"Higareda Almaraz","first_name":"Juan"},{"full_name":"Karbiener, Michael","last_name":"Karbiener","first_name":"Michael"},{"full_name":"Giroud, Maude","last_name":"Giroud","first_name":"Maude"},{"last_name":"Pauler","full_name":"Pauler, Florian","orcid":"0000-0002-7462-0048","first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Gerhalter, Teresa","last_name":"Gerhalter","first_name":"Teresa"},{"last_name":"Herzig","full_name":"Herzig, Stephan","first_name":"Stephan"},{"last_name":"Scheideler","full_name":"Scheideler, Marcel","first_name":"Marcel"}],"publist_id":"8035","external_id":{"isi":["000450976700002"]},"article_processing_charge":"No","title":"Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes"},{"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Table S1. Genes with highest betweenness. Table S2. Local and Master regulators up-regulated. Table S3. Local and Master regulators down-regulated (XLSX 23 kb)."}],"month":"11","oa":1,"main_file_link":[{"open_access":"1","url":"https://doi.org/10.6084/m9.figshare.7295339.v1"}],"publisher":"Springer Nature","day":"03","year":"2018","date_created":"2021-08-06T12:26:53Z","date_published":"2018-11-03T00:00:00Z","doi":"10.6084/m9.figshare.7295339.v1","related_material":{"record":[{"status":"public","id":"20","relation":"used_in_publication"}]},"_id":"9807","status":"public","type":"research_data_reference","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","citation":{"mla":"Higareda Almaraz, Juan, et al. Additional File 1: Of Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes. Springer Nature, 2018, doi:10.6084/m9.figshare.7295339.v1.","ieee":"J. Higareda Almaraz et al., “Additional file 1: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes.” Springer Nature, 2018.","short":"J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S. Herzig, M. Scheideler, (2018).","apa":"Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T., Herzig, S., & Scheideler, M. (2018). Additional file 1: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. Springer Nature. https://doi.org/10.6084/m9.figshare.7295339.v1","ama":"Higareda Almaraz J, Karbiener M, Giroud M, et al. Additional file 1: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. 2018. doi:10.6084/m9.figshare.7295339.v1","chicago":"Higareda Almaraz, Juan, Michael Karbiener, Maude Giroud, Florian Pauler, Teresa Gerhalter, Stephan Herzig, and Marcel Scheideler. “Additional File 1: Of Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes.” Springer Nature, 2018. https://doi.org/10.6084/m9.figshare.7295339.v1.","ista":"Higareda Almaraz J, Karbiener M, Giroud M, Pauler F, Gerhalter T, Herzig S, Scheideler M. 2018. Additional file 1: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes, Springer Nature, 10.6084/m9.figshare.7295339.v1."},"date_updated":"2023-09-13T09:10:47Z","title":"Additional file 1: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes","department":[{"_id":"SiHi"}],"article_processing_charge":"No","author":[{"first_name":"Juan","last_name":"Higareda Almaraz","full_name":"Higareda Almaraz, Juan"},{"first_name":"Michael","full_name":"Karbiener, Michael","last_name":"Karbiener"},{"last_name":"Giroud","full_name":"Giroud, Maude","first_name":"Maude"},{"last_name":"Pauler","orcid":"0000-0002-7462-0048","full_name":"Pauler, Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","first_name":"Florian"},{"full_name":"Gerhalter, Teresa","last_name":"Gerhalter","first_name":"Teresa"},{"first_name":"Stephan","last_name":"Herzig","full_name":"Herzig, Stephan"},{"full_name":"Scheideler, Marcel","last_name":"Scheideler","first_name":"Marcel"}]},{"user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","date_updated":"2023-09-13T09:10:47Z","citation":{"mla":"Higareda Almaraz, Juan, et al. Additional File 3: Of Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes. Springer Nature, 2018, doi:10.6084/m9.figshare.7295369.v1.","ama":"Higareda Almaraz J, Karbiener M, Giroud M, et al. Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. 2018. doi:10.6084/m9.figshare.7295369.v1","apa":"Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T., Herzig, S., & Scheideler, M. (2018). Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. Springer Nature. https://doi.org/10.6084/m9.figshare.7295369.v1","short":"J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S. Herzig, M. Scheideler, (2018).","ieee":"J. Higareda Almaraz et al., “Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes.” Springer Nature, 2018.","chicago":"Higareda Almaraz, Juan, Michael Karbiener, Maude Giroud, Florian Pauler, Teresa Gerhalter, Stephan Herzig, and Marcel Scheideler. “Additional File 3: Of Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes.” Springer Nature, 2018. https://doi.org/10.6084/m9.figshare.7295369.v1.","ista":"Higareda Almaraz J, Karbiener M, Giroud M, Pauler F, Gerhalter T, Herzig S, Scheideler M. 2018. Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes, Springer Nature, 10.6084/m9.figshare.7295369.v1."},"department":[{"_id":"SiHi"}],"title":"Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes","article_processing_charge":"No","author":[{"full_name":"Higareda Almaraz, Juan","last_name":"Higareda Almaraz","first_name":"Juan"},{"full_name":"Karbiener, Michael","last_name":"Karbiener","first_name":"Michael"},{"first_name":"Maude","full_name":"Giroud, Maude","last_name":"Giroud"},{"first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7462-0048","full_name":"Pauler, Florian","last_name":"Pauler"},{"first_name":"Teresa","last_name":"Gerhalter","full_name":"Gerhalter, Teresa"},{"full_name":"Herzig, Stephan","last_name":"Herzig","first_name":"Stephan"},{"last_name":"Scheideler","full_name":"Scheideler, Marcel","first_name":"Marcel"}],"_id":"9808","status":"public","type":"research_data_reference","day":"03","year":"2018","date_created":"2021-08-06T12:31:57Z","related_material":{"record":[{"relation":"used_in_publication","id":"20","status":"public"}]},"date_published":"2018-11-03T00:00:00Z","doi":"10.6084/m9.figshare.7295369.v1","oa_version":"Published Version","abstract":[{"lang":"eng","text":"Table S4. Counts per Gene per Million Reads Mapped. (XLSX 2751 kb)."}],"month":"11","main_file_link":[{"open_access":"1","url":"https://doi.org/10.6084/m9.figshare.7295369.v1"}],"oa":1,"publisher":"Springer Nature"},{"month":"11","alternative_title":["ISTA Thesis"],"oa_version":"Published Version","abstract":[{"text":"Genomic imprinting is an epigenetic process that leads to parent of origin-specific gene expression in a subset of genes. Imprinted genes are essential for brain development, and deregulation of imprinting is associated with neurodevelopmental diseases and the pathogenesis of psychiatric disorders. However, the cell-type specificity of imprinting at single cell resolution, and how imprinting and thus gene dosage regulates neuronal circuit assembly is still largely unknown. Here, MADM (Mosaic Analysis with Double Markers) technology was employed to assess genomic imprinting at single cell level. By visualizing MADM-induced uniparental disomies (UPDs) in distinct colors at single cell level in genetic mosaic animals, this experimental paradigm provides a unique quantitative platform to systematically assay the UPD-mediated imbalances in imprinted gene expression at unprecedented resolution. An experimental pipeline based on FACS, RNA-seq and bioinformatics analysis was established and applied to systematically map cell-type-specific ‘imprintomes’ in the mouse brain. The results revealed that parental-specific expression of imprinted genes per se is rarely cell-type-specific even at the individual cell level. Conversely, when we extended the comparison to downstream responses resulting from imbalanced imprinted gene expression, we discovered an unexpectedly high degree of cell-type specificity. Furthermore, we determined a novel function of genomic imprinting in cortical astrocyte production and in olfactory bulb (OB) granule cell generation. These results suggest important functional implication of genomic imprinting for generating cell-type diversity in the brain. In addition, MADM provides a powerful tool to study candidate genes by concomitant genetic manipulation and fluorescent labelling of single cells. MADM-based candidate gene approach was utilized to identify potential imprinted genes involved in the generation of cortical astrocytes and OB granule cells. We investigated p57Kip2, a maternally expressed gene and known cell cycle regulator. Although we found that p57Kip2 does not play a role in these processes, we detected an unexpected function of the paternal allele previously thought to be silent. Finally, we took advantage of a key property of MADM which is to allow unambiguous investigation of environmental impact on single cells. The experimental pipeline based on FACS and RNA-seq analysis of MADM-labeled cells was established to probe the functional differences of single cell loss of gene function compared to global loss of function on a transcriptional level. With this method, both common and distinct responses were isolated due to cell-autonomous and non-autonomous effects acting on genotypically identical cells. As a result, transcriptional changes were identified which result solely from the surrounding environment. Using the MADM technology to study genomic imprinting at single cell resolution, we have identified cell-type-specific gene expression, novel gene function and the impact of environment on single cell transcriptomes. Together, these provide important insights to the understanding of mechanisms regulating cell-type specificity and thus diversity in the brain.","lang":"eng"}],"file":[{"file_name":"Thesis_LaukoterSusanne_FINAL.docx","date_created":"2019-05-10T07:47:04Z","file_size":17949175,"date_updated":"2019-11-23T23:30:03Z","creator":"dernst","file_id":"6396","checksum":"41fdbf5fdce312802935d88a8ad9932c","embargo_to":"open_access","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","relation":"source_file","access_level":"closed"},{"date_updated":"2021-02-11T11:17:16Z","file_size":21187245,"creator":"dernst","date_created":"2019-05-10T07:47:04Z","file_name":"Thesis_LaukoterSusanne_FINAL.pdf","content_type":"application/pdf","access_level":"open_access","relation":"main_file","checksum":"53001a9a0c9e570e598d861bb0af28aa","file_id":"6397","embargo":"2019-11-21"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2663-337X"]},"publication_status":"published","degree_awarded":"PhD","status":"public","pubrep_id":"1057","type":"dissertation","_id":"10","file_date_updated":"2021-02-11T11:17:16Z","department":[{"_id":"SiHi"}],"ddc":["570"],"supervisor":[{"last_name":"Vicoso","orcid":"0000-0002-4579-8306","full_name":"Vicoso, Beatriz","id":"49E1C5C6-F248-11E8-B48F-1D18A9856A87","first_name":"Beatriz"}],"date_updated":"2023-09-07T12:40:44Z","publisher":"Institute of Science and Technology Austria","oa":1,"date_published":"2018-11-21T00:00:00Z","doi":"10.15479/AT:ISTA:th1057","date_created":"2018-12-11T11:44:08Z","page":"1 - 139","day":"21","has_accepted_license":"1","year":"2018","title":"Role of genomic imprinting in cerebral cortex development","publist_id":"8046","author":[{"orcid":"0000-0002-7903-3010","full_name":"Laukoter, Susanne","last_name":"Laukoter","first_name":"Susanne","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87"}],"article_processing_charge":"No","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"mla":"Laukoter, Susanne. Role of Genomic Imprinting in Cerebral Cortex Development. Institute of Science and Technology Austria, 2018, pp. 1–139, doi:10.15479/AT:ISTA:th1057.","ama":"Laukoter S. Role of genomic imprinting in cerebral cortex development. 2018:1-139. doi:10.15479/AT:ISTA:th1057","apa":"Laukoter, S. (2018). Role of genomic imprinting in cerebral cortex development. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th1057","short":"S. Laukoter, Role of Genomic Imprinting in Cerebral Cortex Development, Institute of Science and Technology Austria, 2018.","ieee":"S. Laukoter, “Role of genomic imprinting in cerebral cortex development,” Institute of Science and Technology Austria, 2018.","chicago":"Laukoter, Susanne. “Role of Genomic Imprinting in Cerebral Cortex Development.” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th1057.","ista":"Laukoter S. 2018. Role of genomic imprinting in cerebral cortex development. Institute of Science and Technology Austria."}},{"citation":{"mla":"Contreras, Ximena, and Simon Hippenmeyer. “Incorrect Trafficking Route Leads to Autism.” Brain a Journal of Neurology, vol. 141, no. 9, Oxford University Press, 2018, pp. 2542–44, doi:10.1093/brain/awy218.","short":"X. Contreras, S. Hippenmeyer, Brain a Journal of Neurology 141 (2018) 2542–2544.","ieee":"X. Contreras and S. Hippenmeyer, “Incorrect trafficking route leads to autism,” Brain a journal of neurology, vol. 141, no. 9. Oxford University Press, pp. 2542–2544, 2018.","ama":"Contreras X, Hippenmeyer S. Incorrect trafficking route leads to autism. Brain a journal of neurology. 2018;141(9):2542-2544. doi:10.1093/brain/awy218","apa":"Contreras, X., & Hippenmeyer, S. (2018). Incorrect trafficking route leads to autism. Brain a Journal of Neurology. Oxford University Press. https://doi.org/10.1093/brain/awy218","chicago":"Contreras, Ximena, and Simon Hippenmeyer. “Incorrect Trafficking Route Leads to Autism.” Brain a Journal of Neurology. Oxford University Press, 2018. https://doi.org/10.1093/brain/awy218.","ista":"Contreras X, Hippenmeyer S. 2018. Incorrect trafficking route leads to autism. Brain a journal of neurology. 141(9), 2542–2544."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","external_id":{"isi":["000446548100012"]},"article_processing_charge":"No","author":[{"last_name":"Contreras","full_name":"Contreras, Ximena","id":"475990FE-F248-11E8-B48F-1D18A9856A87","first_name":"Ximena"},{"last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"title":"Incorrect trafficking route leads to autism","year":"2018","isi":1,"publication":"Brain a journal of neurology","day":"01","page":"2542 - 2544","date_created":"2018-12-11T11:44:14Z","date_published":"2018-09-01T00:00:00Z","doi":"10.1093/brain/awy218","publisher":"Oxford University Press","quality_controlled":"1","date_updated":"2024-03-27T23:30:41Z","department":[{"_id":"SiHi"}],"_id":"28","type":"journal_article","status":"public","publication_status":"published","language":[{"iso":"eng"}],"issue":"9","volume":141,"related_material":{"record":[{"relation":"part_of_dissertation","id":"7902","status":"public"}]},"abstract":[{"text":"This scientific commentary refers to ‘NEGR1 and FGFR2 cooperatively regulate cortical development and core behaviours related to autism disorders in mice’ by Szczurkowska et al. ","lang":"eng"}],"oa_version":"None","scopus_import":"1","intvolume":" 141","month":"09"},{"project":[{"name":"Revealing the mechanisms underlying drug interactions","grant_number":"P27201-B22","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"article_number":"e25125","title":"Mapping the mouse Allelome reveals tissue specific regulation of allelic expression","author":[{"first_name":"Daniel","full_name":"Andergassen, Daniel","last_name":"Andergassen"},{"full_name":"Dotter, Christoph","last_name":"Dotter","first_name":"Christoph","id":"4C66542E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Wenzel, Dyniel","last_name":"Wenzel","first_name":"Dyniel"},{"last_name":"Sigl","full_name":"Sigl, Verena","first_name":"Verena"},{"full_name":"Bammer, Philipp","last_name":"Bammer","first_name":"Philipp"},{"first_name":"Markus","full_name":"Muckenhuber, Markus","last_name":"Muckenhuber"},{"last_name":"Mayer","full_name":"Mayer, Daniela","first_name":"Daniela"},{"first_name":"Tomasz","full_name":"Kulinski, Tomasz","last_name":"Kulinski"},{"first_name":"Hans","full_name":"Theussl, Hans","last_name":"Theussl"},{"first_name":"Josef","full_name":"Penninger, Josef","last_name":"Penninger"},{"full_name":"Bock, Christoph","last_name":"Bock","first_name":"Christoph"},{"full_name":"Barlow, Denise","last_name":"Barlow","first_name":"Denise"},{"first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","last_name":"Pauler"},{"first_name":"Quanah","full_name":"Hudson, Quanah","last_name":"Hudson"}],"publist_id":"6971","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Andergassen, Daniel, Christoph Dotter, Dyniel Wenzel, Verena Sigl, Philipp Bammer, Markus Muckenhuber, Daniela Mayer, et al. “Mapping the Mouse Allelome Reveals Tissue Specific Regulation of Allelic Expression.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.25125.","ista":"Andergassen D, Dotter C, Wenzel D, Sigl V, Bammer P, Muckenhuber M, Mayer D, Kulinski T, Theussl H, Penninger J, Bock C, Barlow D, Pauler F, Hudson Q. 2017. Mapping the mouse Allelome reveals tissue specific regulation of allelic expression. eLife. 6, e25125.","mla":"Andergassen, Daniel, et al. “Mapping the Mouse Allelome Reveals Tissue Specific Regulation of Allelic Expression.” ELife, vol. 6, e25125, eLife Sciences Publications, 2017, doi:10.7554/eLife.25125.","ama":"Andergassen D, Dotter C, Wenzel D, et al. Mapping the mouse Allelome reveals tissue specific regulation of allelic expression. eLife. 2017;6. doi:10.7554/eLife.25125","apa":"Andergassen, D., Dotter, C., Wenzel, D., Sigl, V., Bammer, P., Muckenhuber, M., … Hudson, Q. (2017). Mapping the mouse Allelome reveals tissue specific regulation of allelic expression. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.25125","short":"D. Andergassen, C. Dotter, D. Wenzel, V. Sigl, P. Bammer, M. Muckenhuber, D. Mayer, T. Kulinski, H. Theussl, J. Penninger, C. Bock, D. Barlow, F. Pauler, Q. Hudson, ELife 6 (2017).","ieee":"D. Andergassen et al., “Mapping the mouse Allelome reveals tissue specific regulation of allelic expression,” eLife, vol. 6. eLife Sciences Publications, 2017."},"publisher":"eLife Sciences Publications","quality_controlled":"1","oa":1,"doi":"10.7554/eLife.25125","date_published":"2017-08-14T00:00:00Z","date_created":"2018-12-11T11:48:05Z","day":"14","publication":"eLife","has_accepted_license":"1","year":"2017","status":"public","pubrep_id":"885","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"713","file_date_updated":"2020-07-14T12:47:50Z","department":[{"_id":"GaNo"},{"_id":"SiHi"}],"ddc":["576"],"date_updated":"2021-01-12T08:11:57Z","month":"08","intvolume":" 6","scopus_import":1,"oa_version":"Published Version","abstract":[{"text":"To determine the dynamics of allelic-specific expression during mouse development, we analyzed RNA-seq data from 23 F1 tissues from different developmental stages, including 19 female tissues allowing X chromosome inactivation (XCI) escapers to also be detected. We demonstrate that allelic expression arising from genetic or epigenetic differences is highly tissue-specific. We find that tissue-specific strain-biased gene expression may be regulated by tissue-specific enhancers or by post-transcriptional differences in stability between the alleles. We also find that escape from X-inactivation is tissue-specific, with leg muscle showing an unexpectedly high rate of XCI escapers. By surveying a range of tissues during development, and performing extensive validation, we are able to provide a high confidence list of mouse imprinted genes including 18 novel genes. This shows that cluster size varies dynamically during development and can be substantially larger than previously thought, with the Igf2r cluster extending over 10 Mb in placenta.","lang":"eng"}],"volume":6,"file":[{"relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_id":"5020","checksum":"1ace3462e64a971b9ead896091829549","creator":"system","file_size":6399510,"date_updated":"2020-07-14T12:47:50Z","file_name":"IST-2017-885-v1+1_elife-25125-figures-v2.pdf","date_created":"2018-12-12T10:13:36Z"},{"content_type":"application/pdf","access_level":"open_access","relation":"main_file","file_id":"5021","checksum":"6241dc31eeb87b03facadec3a53a6827","date_updated":"2020-07-14T12:47:50Z","file_size":4264398,"creator":"system","date_created":"2018-12-12T10:13:36Z","file_name":"IST-2017-885-v1+2_elife-25125-v2.pdf"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2050084X"]},"publication_status":"published"},{"user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","date_updated":"2022-08-25T13:34:55Z","citation":{"ista":"Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. 2017. Data from: Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis, Dryad, 10.5061/dryad.pk16b.","chicago":"Riccio, Paul, Christina Cebrián, Hui Zong, Simon Hippenmeyer, and Frank Costantini. “Data from: Ret and Etv4 Promote Directed Movements of Progenitor Cells during Renal Branching Morphogenesis.” Dryad, 2017. https://doi.org/10.5061/dryad.pk16b.","apa":"Riccio, P., Cebrián, C., Zong, H., Hippenmeyer, S., & Costantini, F. (2017). Data from: Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis. Dryad. https://doi.org/10.5061/dryad.pk16b","ama":"Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. Data from: Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis. 2017. doi:10.5061/dryad.pk16b","ieee":"P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, and F. Costantini, “Data from: Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis.” Dryad, 2017.","short":"P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, F. Costantini, (2017).","mla":"Riccio, Paul, et al. Data from: Ret and Etv4 Promote Directed Movements of Progenitor Cells during Renal Branching Morphogenesis. Dryad, 2017, doi:10.5061/dryad.pk16b."},"department":[{"_id":"SiHi"}],"title":"Data from: Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis","article_processing_charge":"No","author":[{"first_name":"Paul","last_name":"Riccio","full_name":"Riccio, Paul"},{"full_name":"Cebrián, Christina","last_name":"Cebrián","first_name":"Christina"},{"full_name":"Zong, Hui","last_name":"Zong","first_name":"Hui"},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Costantini, Frank","last_name":"Costantini","first_name":"Frank"}],"_id":"9707","status":"public","type":"research_data_reference","day":"14","year":"2017","date_created":"2021-07-23T09:39:34Z","date_published":"2017-01-14T00:00:00Z","doi":"10.5061/dryad.pk16b","related_material":{"record":[{"id":"9702","status":"deleted","relation":"used_in_publication"}]},"oa_version":"Published Version","abstract":[{"text":"Branching morphogenesis of the epithelial ureteric bud forms the renal collecting duct system and is critical for normal nephron number, while low nephron number is implicated in hypertension and renal disease. Ureteric bud growth and branching requires GDNF signaling from the surrounding mesenchyme to cells at the ureteric bud tips, via the Ret receptor tyrosine kinase and coreceptor Gfrα1; Ret signaling up-regulates transcription factors Etv4 and Etv5, which are also critical for branching. Despite extensive knowledge of the genetic control of these events, it is not understood, at the cellular level, how renal branching morphogenesis is achieved or how Ret signaling influences epithelial cell behaviors to promote this process. Analysis of chimeric embryos previously suggested a role for Ret signaling in promoting cell rearrangements in the nephric duct, but this method was unsuited to study individual cell behaviors during ureteric bud branching. Here, we use Mosaic Analysis with Double Markers (MADM), combined with organ culture and time-lapse imaging, to trace the movements and divisions of individual ureteric bud tip cells. We first examine wild-type clones and then Ret or Etv4 mutant/wild-type clones in which the mutant and wild-type sister cells are differentially and heritably marked by green and red fluorescent proteins. We find that, in normal kidneys, most individual tip cells behave as self-renewing progenitors, some of whose progeny remain at the tips while others populate the growing UB trunks. In Ret or Etv4 MADM clones, the wild-type cells generated at a UB tip are much more likely to remain at, or move to, the new tips during branching and elongation, while their Ret−/− or Etv4−/− sister cells tend to lag behind and contribute only to the trunks. By tracking successive mitoses in a cell lineage, we find that Ret signaling has little effect on proliferation, in contrast to its effects on cell movement. Our results show that Ret/Etv4 signaling promotes directed cell movements in the ureteric bud tips, and suggest a model in which these cell movements mediate branching morphogenesis.","lang":"eng"}],"month":"01","main_file_link":[{"open_access":"1","url":"https://doi.org/10.5061/dryad.pk16b"}],"oa":1,"publisher":"Dryad"},{"language":[{"iso":"eng"}],"file":[{"content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_id":"4742","file_size":1436377,"date_updated":"2018-12-12T10:09:19Z","creator":"system","file_name":"IST-2017-806-v1+2_1-s2.0-S1044743116302500-main_1_.pdf","date_created":"2018-12-12T10:09:19Z"}],"publication_status":"published","publication_identifier":{"issn":["10447431"]},"volume":84,"oa_version":"Published Version","abstract":[{"lang":"eng","text":"The development of the vertebrate central nervous system is reliant on a complex cascade of biological processes that include mitotic division, relocation of migrating neurons, and the extension of dendritic and axonal processes. Each of these cellular events requires the diverse functional repertoire of the microtubule cytoskeleton for the generation of forces, assembly of macromolecular complexes and transport of molecules and organelles. The tubulins are a multi-gene family that encode for the constituents of microtubules, and have been implicated in a spectrum of neurological disorders. Evidence is building that different tubulins tune the functional properties of the microtubule cytoskeleton dependent on the cell type, developmental profile and subcellular localisation. Here we review of the origins of the functional specification of the tubulin gene family in the developing brain at a transcriptional, translational, and post-transcriptional level. We remind the reader that tubulins are not just loading controls for your average Western blot."}],"intvolume":" 84","month":"10","scopus_import":"1","ddc":["571"],"date_updated":"2023-09-22T09:42:15Z","file_date_updated":"2018-12-12T10:09:19Z","department":[{"_id":"SiHi"}],"_id":"1017","pubrep_id":"806","status":"public","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"type":"journal_article","publication":"Molecular and Cellular Neuroscience","day":"01","year":"2017","has_accepted_license":"1","isi":1,"date_created":"2018-12-11T11:49:42Z","doi":"10.1016/j.mcn.2017.03.002","date_published":"2017-10-01T00:00:00Z","page":"58 - 67","oa":1,"quality_controlled":"1","publisher":"Academic Press","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"mla":"Breuss, Martin, et al. “Tubulins and Brain Development: The Origins of Functional Specification.” Molecular and Cellular Neuroscience, vol. 84, Academic Press, 2017, pp. 58–67, doi:10.1016/j.mcn.2017.03.002.","ama":"Breuss M, Leca I, Gstrein T, Hansen AH, Keays D. Tubulins and brain development: The origins of functional specification. Molecular and Cellular Neuroscience. 2017;84:58-67. doi:10.1016/j.mcn.2017.03.002","apa":"Breuss, M., Leca, I., Gstrein, T., Hansen, A. H., & Keays, D. (2017). Tubulins and brain development: The origins of functional specification. Molecular and Cellular Neuroscience. Academic Press. https://doi.org/10.1016/j.mcn.2017.03.002","short":"M. Breuss, I. Leca, T. Gstrein, A.H. Hansen, D. Keays, Molecular and Cellular Neuroscience 84 (2017) 58–67.","ieee":"M. Breuss, I. Leca, T. Gstrein, A. H. Hansen, and D. Keays, “Tubulins and brain development: The origins of functional specification,” Molecular and Cellular Neuroscience, vol. 84. Academic Press, pp. 58–67, 2017.","chicago":"Breuss, Martin, Ines Leca, Thomas Gstrein, Andi H Hansen, and David Keays. “Tubulins and Brain Development: The Origins of Functional Specification.” Molecular and Cellular Neuroscience. Academic Press, 2017. https://doi.org/10.1016/j.mcn.2017.03.002.","ista":"Breuss M, Leca I, Gstrein T, Hansen AH, Keays D. 2017. Tubulins and brain development: The origins of functional specification. Molecular and Cellular Neuroscience. 84, 58–67."},"title":"Tubulins and brain development: The origins of functional specification","article_processing_charge":"No","external_id":{"isi":["000415140700007"]},"publist_id":"6377","author":[{"full_name":"Breuss, Martin","last_name":"Breuss","first_name":"Martin"},{"full_name":"Leca, Ines","last_name":"Leca","first_name":"Ines"},{"first_name":"Thomas","last_name":"Gstrein","full_name":"Gstrein, Thomas"},{"full_name":"Hansen, Andi H","last_name":"Hansen","first_name":"Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87"},{"first_name":"David","last_name":"Keays","full_name":"Keays, David"}]},{"volume":26,"issue":"2","language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"issn":["09646906"]},"intvolume":" 26","month":"01","scopus_import":"1","oa_version":"None","abstract":[{"lang":"eng","text":"The integrity and dynamic properties of the microtubule cytoskeleton are indispensable for the development of the mammalian brain. Consequently, mutations in the genes that encode the structural component (the α/β-tubulin heterodimer) can give rise to severe, sporadic neurodevelopmental disorders. These are commonly referred to as the tubulinopathies. Here we report the addition of recessive quadrupedalism, also known as Uner Tan syndrome (UTS), to the growing list of diseases caused by tubulin variants. Analysis of a consanguineous UTS family identified a biallelic TUBB2B mutation, resulting in a p.R390Q amino acid substitution. In addition to the identifying quadrupedal locomotion, all three patients showed severe cerebellar hypoplasia. None, however, displayed the basal ganglia malformations typically associated with TUBB2B mutations. Functional analysis of the R390Q substitution revealed that it did not affect the ability of β-tubulin to fold or become assembled into the α/β-heterodimer, nor did it influence the incorporation of mutant-containing heterodimers into microtubule polymers. The 390Q mutation in S. cerevisiae TUB2 did not affect growth under basal conditions, but did result in increased sensitivity to microtubule-depolymerizing drugs, indicative of a mild impact of this mutation on microtubule function. The TUBB2B mutation described here represents an unusual recessive mode of inheritance for missense-mediated tubulinopathies and reinforces the sensitivity of the developing cerebellum to microtubule defects."}],"department":[{"_id":"SiHi"}],"date_updated":"2023-09-22T09:42:42Z","status":"public","type":"journal_article","_id":"1016","date_created":"2018-12-11T11:49:42Z","date_published":"2017-01-01T00:00:00Z","doi":"10.1093/hmg/ddw383","page":"258 - 269","publication":"Human Molecular Genetics","day":"01","year":"2017","isi":1,"publisher":"Oxford University Press","quality_controlled":"1","title":"Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability","article_processing_charge":"No","external_id":{"isi":["000397066400002"]},"publist_id":"6379","author":[{"last_name":"Breuss","full_name":"Breuss, Martin","first_name":"Martin"},{"full_name":"Nguyen, Thai","last_name":"Nguyen","first_name":"Thai"},{"first_name":"Anjana","last_name":"Srivatsan","full_name":"Srivatsan, Anjana"},{"last_name":"Leca","full_name":"Leca, Ines","first_name":"Ines"},{"last_name":"Tian","full_name":"Tian, Guoling","first_name":"Guoling"},{"full_name":"Fritz, Tanja","last_name":"Fritz","first_name":"Tanja"},{"full_name":"Hansen, Andi H","last_name":"Hansen","first_name":"Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Damir","full_name":"Musaev, Damir","last_name":"Musaev"},{"full_name":"Mcevoy Venneri, Jennifer","last_name":"Mcevoy Venneri","first_name":"Jennifer"},{"full_name":"Kiely, James","last_name":"Kiely","first_name":"James"},{"full_name":"Rosti, Rasim","last_name":"Rosti","first_name":"Rasim"},{"first_name":"Eric","last_name":"Scott","full_name":"Scott, Eric"},{"first_name":"Uner","full_name":"Tan, Uner","last_name":"Tan"},{"full_name":"Kolodner, Richard","last_name":"Kolodner","first_name":"Richard"},{"first_name":"Nicholas","last_name":"Cowan","full_name":"Cowan, Nicholas"},{"last_name":"Keays","full_name":"Keays, David","first_name":"David"},{"last_name":"Gleeson","full_name":"Gleeson, Joseph","first_name":"Joseph"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"ista":"Breuss M, Nguyen T, Srivatsan A, Leca I, Tian G, Fritz T, Hansen AH, Musaev D, Mcevoy Venneri J, Kiely J, Rosti R, Scott E, Tan U, Kolodner R, Cowan N, Keays D, Gleeson J. 2017. Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability. Human Molecular Genetics. 26(2), 258–269.","chicago":"Breuss, Martin, Thai Nguyen, Anjana Srivatsan, Ines Leca, Guoling Tian, Tanja Fritz, Andi H Hansen, et al. “Uner Tan Syndrome Caused by a Homozygous TUBB2B Mutation Affecting Microtubule Stability.” Human Molecular Genetics. Oxford University Press, 2017. https://doi.org/10.1093/hmg/ddw383.","ama":"Breuss M, Nguyen T, Srivatsan A, et al. Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability. Human Molecular Genetics. 2017;26(2):258-269. doi:10.1093/hmg/ddw383","apa":"Breuss, M., Nguyen, T., Srivatsan, A., Leca, I., Tian, G., Fritz, T., … Gleeson, J. (2017). Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability. Human Molecular Genetics. Oxford University Press. https://doi.org/10.1093/hmg/ddw383","ieee":"M. Breuss et al., “Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability,” Human Molecular Genetics, vol. 26, no. 2. Oxford University Press, pp. 258–269, 2017.","short":"M. Breuss, T. Nguyen, A. Srivatsan, I. Leca, G. Tian, T. Fritz, A.H. Hansen, D. Musaev, J. Mcevoy Venneri, J. Kiely, R. Rosti, E. Scott, U. Tan, R. Kolodner, N. Cowan, D. Keays, J. Gleeson, Human Molecular Genetics 26 (2017) 258–269.","mla":"Breuss, Martin, et al. “Uner Tan Syndrome Caused by a Homozygous TUBB2B Mutation Affecting Microtubule Stability.” Human Molecular Genetics, vol. 26, no. 2, Oxford University Press, 2017, pp. 258–69, doi:10.1093/hmg/ddw383."}},{"project":[{"call_identifier":"FP7","_id":"25D61E48-B435-11E9-9278-68D0E5697425","grant_number":"618444","name":"Molecular Mechanisms of Cerebral Cortex Development"},{"grant_number":"RGP0053/2014","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level","_id":"25D7962E-B435-11E9-9278-68D0E5697425"}],"citation":{"ama":"Beattie RJ, Postiglione MP, Burnett L, et al. Mosaic analysis with double markers reveals distinct sequential functions of Lgl1 in neural stem cells. Neuron. 2017;94(3):517-533.e3. doi:10.1016/j.neuron.2017.04.012","apa":"Beattie, R. J., Postiglione, M. P., Burnett, L., Laukoter, S., Streicher, C., Pauler, F., … Hippenmeyer, S. (2017). Mosaic analysis with double markers reveals distinct sequential functions of Lgl1 in neural stem cells. Neuron. Cell Press. https://doi.org/10.1016/j.neuron.2017.04.012","ieee":"R. J. Beattie et al., “Mosaic analysis with double markers reveals distinct sequential functions of Lgl1 in neural stem cells,” Neuron, vol. 94, no. 3. Cell Press, p. 517–533.e3, 2017.","short":"R.J. Beattie, M.P. Postiglione, L. Burnett, S. Laukoter, C. Streicher, F. Pauler, G. Xiao, O. Klezovitch, V. Vasioukhin, T. Ghashghaei, S. Hippenmeyer, Neuron 94 (2017) 517–533.e3.","mla":"Beattie, Robert J., et al. “Mosaic Analysis with Double Markers Reveals Distinct Sequential Functions of Lgl1 in Neural Stem Cells.” Neuron, vol. 94, no. 3, Cell Press, 2017, p. 517–533.e3, doi:10.1016/j.neuron.2017.04.012.","ista":"Beattie RJ, Postiglione MP, Burnett L, Laukoter S, Streicher C, Pauler F, Xiao G, Klezovitch O, Vasioukhin V, Ghashghaei T, Hippenmeyer S. 2017. Mosaic analysis with double markers reveals distinct sequential functions of Lgl1 in neural stem cells. Neuron. 94(3), 517–533.e3.","chicago":"Beattie, Robert J, Maria P Postiglione, Laura Burnett, Susanne Laukoter, Carmen Streicher, Florian Pauler, Guanxi Xiao, et al. “Mosaic Analysis with Double Markers Reveals Distinct Sequential Functions of Lgl1 in Neural Stem Cells.” Neuron. Cell Press, 2017. https://doi.org/10.1016/j.neuron.2017.04.012."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","external_id":{"isi":["000400466700011"]},"article_processing_charge":"No","author":[{"full_name":"Beattie, Robert J","orcid":"0000-0002-8483-8753","last_name":"Beattie","first_name":"Robert J","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Postiglione","full_name":"Postiglione, Maria P","first_name":"Maria P","id":"2C67902A-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0002-8937-410X","full_name":"Burnett, Laura","last_name":"Burnett","first_name":"Laura","id":"3B717F68-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Laukoter","orcid":"0000-0002-7903-3010","full_name":"Laukoter, Susanne","first_name":"Susanne","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Streicher, Carmen","last_name":"Streicher","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","first_name":"Carmen"},{"first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","last_name":"Pauler","full_name":"Pauler, Florian","orcid":"0000-0002-7462-0048"},{"last_name":"Xiao","full_name":"Xiao, Guanxi","first_name":"Guanxi"},{"first_name":"Olga","last_name":"Klezovitch","full_name":"Klezovitch, Olga"},{"first_name":"Valeri","full_name":"Vasioukhin, Valeri","last_name":"Vasioukhin"},{"first_name":"Troy","last_name":"Ghashghaei","full_name":"Ghashghaei, Troy"},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"publist_id":"6473","title":"Mosaic analysis with double markers reveals distinct sequential functions of Lgl1 in neural stem cells","publisher":"Cell Press","quality_controlled":"1","year":"2017","isi":1,"publication":"Neuron","day":"03","page":"517 - 533.e3","date_created":"2018-12-11T11:49:20Z","date_published":"2017-05-03T00:00:00Z","doi":"10.1016/j.neuron.2017.04.012","_id":"944","type":"journal_article","status":"public","date_updated":"2023-09-26T15:37:02Z","department":[{"_id":"SiHi"},{"_id":"MaJö"}],"abstract":[{"text":"The concerted production of neurons and glia by neural stem cells (NSCs) is essential for neural circuit assembly. In the developing cerebral cortex, radial glia progenitors (RGPs) generate nearly all neocortical neurons and certain glia lineages. RGP proliferation behavior shows a high degree of non-stochasticity, thus a deterministic characteristic of neuron and glia production. However, the cellular and molecular mechanisms controlling RGP behavior and proliferation dynamics in neurogenesis and glia generation remain unknown. By using mosaic analysis with double markers (MADM)-based genetic paradigms enabling the sparse and global knockout with unprecedented single-cell resolution, we identified Lgl1 as a critical regulatory component. We uncover Lgl1-dependent tissue-wide community effects required for embryonic cortical neurogenesis and novel cell-autonomous Lgl1 functions controlling RGP-mediated glia genesis and postnatal NSC behavior. These results suggest that NSC-mediated neuron and glia production is tightly regulated through the concerted interplay of sequential Lgl1-dependent global and cell intrinsic mechanisms.","lang":"eng"}],"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"oa_version":"None","scopus_import":"1","intvolume":" 94","month":"05","publication_status":"published","publication_identifier":{"issn":["08966273"]},"language":[{"iso":"eng"}],"ec_funded":1,"issue":"3","volume":94},{"oa_version":"None","abstract":[{"lang":"eng","text":"During corticogenesis, distinct classes of neurons are born from progenitor cells located in the ventricular and subventricular zones, from where they migrate towards the pial surface to assemble into highly organized layer-specific circuits. However, the precise and coordinated transcriptional network activity defining neuronal identity is still not understood. Here, we show that genetic depletion of the basic helix-loop-helix (bHLH) transcription factor E2A splice variant E47 increased the number of Tbr1-positive deep layer and Satb2-positive upper layer neurons at E14.5, while depletion of the alternatively spliced E12 variant did not affect layer-specific neurogenesis. While ChIP-Seq identified a big overlap for E12- and E47-specific binding sites in embryonic NSCs, including sites at the cyclin-dependent kinase inhibitor (CDKI) Cdkn1c gene locus, RNA-Seq revealed a unique transcriptional regulation by each splice variant. E47 activated the expression of the CDKI Cdkn1c through binding to a distal enhancer. Finally, overexpression of E47 in embryonic NSCs in vitro impaired neurite outgrowth and E47 overexpression in vivo by in utero electroporation disturbed proper layer-specific neurogenesis and upregulated p57(KIP2) expression. Overall, this study identified E2A target genes in embryonic NSCs and demonstrates that E47 regulates neuronal differentiation via p57(KIP2)."}],"intvolume":" 144","month":"10","scopus_import":"1","quality_controlled":"1","publisher":"Company of Biologists","language":[{"iso":"eng"}],"publication":"Development","day":"31","publication_status":"published","year":"2017","isi":1,"date_created":"2018-12-11T11:48:36Z","doi":"10.1242/dev.145698","date_published":"2017-10-31T00:00:00Z","volume":144,"page":"3917 - 3931","_id":"805","status":"public","type":"journal_article","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","date_updated":"2023-09-26T16:20:09Z","citation":{"mla":"Pfurr, Sabrina, et al. “The E2A Splice Variant E47 Regulates the Differentiation of Projection Neurons via P57(KIP2) during Cortical Development.” Development, vol. 144, Company of Biologists, 2017, pp. 3917–31, doi:10.1242/dev.145698.","ama":"Pfurr S, Chu Y, Bohrer C, et al. The E2A splice variant E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical development. Development. 2017;144:3917-3931. doi:10.1242/dev.145698","apa":"Pfurr, S., Chu, Y., Bohrer, C., Greulich, F., Beattie, R. J., Mammadzada, K., … Schachtrup, C. (2017). The E2A splice variant E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical development. Development. Company of Biologists. https://doi.org/10.1242/dev.145698","short":"S. Pfurr, Y. Chu, C. Bohrer, F. Greulich, R.J. Beattie, K. Mammadzada, M. Hils, S. Arnold, V. Taylor, K. Schachtrup, N.H. Uhlenhaut, C. Schachtrup, Development 144 (2017) 3917–3931.","ieee":"S. Pfurr et al., “The E2A splice variant E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical development,” Development, vol. 144. Company of Biologists, pp. 3917–3931, 2017.","chicago":"Pfurr, Sabrina, Yu Chu, Christian Bohrer, Franziska Greulich, Robert J Beattie, Könül Mammadzada, Miriam Hils, et al. “The E2A Splice Variant E47 Regulates the Differentiation of Projection Neurons via P57(KIP2) during Cortical Development.” Development. Company of Biologists, 2017. https://doi.org/10.1242/dev.145698.","ista":"Pfurr S, Chu Y, Bohrer C, Greulich F, Beattie RJ, Mammadzada K, Hils M, Arnold S, Taylor V, Schachtrup K, Uhlenhaut NH, Schachtrup C. 2017. The E2A splice variant E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical development. Development. 144, 3917–3931."},"title":"The E2A splice variant E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical development","department":[{"_id":"SiHi"}],"external_id":{"isi":["000414025600007"]},"article_processing_charge":"No","author":[{"first_name":"Sabrina","last_name":"Pfurr","full_name":"Pfurr, Sabrina"},{"full_name":"Chu, Yu","last_name":"Chu","first_name":"Yu"},{"last_name":"Bohrer","full_name":"Bohrer, Christian","first_name":"Christian"},{"last_name":"Greulich","full_name":"Greulich, Franziska","first_name":"Franziska"},{"orcid":"0000-0002-8483-8753","full_name":"Beattie, Robert J","last_name":"Beattie","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","first_name":"Robert J"},{"full_name":"Mammadzada, Könül","last_name":"Mammadzada","first_name":"Könül"},{"first_name":"Miriam","last_name":"Hils","full_name":"Hils, Miriam"},{"first_name":"Sebastian","last_name":"Arnold","full_name":"Arnold, Sebastian"},{"last_name":"Taylor","full_name":"Taylor, Verdon","first_name":"Verdon"},{"last_name":"Schachtrup","full_name":"Schachtrup, Kristina","first_name":"Kristina"},{"first_name":"N Henriette","full_name":"Uhlenhaut, N Henriette","last_name":"Uhlenhaut"},{"first_name":"Christian","last_name":"Schachtrup","full_name":"Schachtrup, Christian"}],"publist_id":"6846"},{"ec_funded":1,"issue":"24","volume":591,"language":[{"iso":"eng"}],"file":[{"date_created":"2018-12-12T10:16:24Z","file_name":"IST-2018-928-v1+1_Beattie_et_al-2017-FEBS_Letters.pdf","creator":"system","date_updated":"2020-07-14T12:47:24Z","file_size":644149,"checksum":"a46dadc84e0c28d389dd3e9e954464db","file_id":"5211","access_level":"open_access","relation":"main_file","content_type":"application/pdf"}],"publication_status":"published","publication_identifier":{"issn":["00145793"]},"intvolume":" 591","month":"12","scopus_import":"1","pmid":1,"oa_version":"Published Version","abstract":[{"lang":"eng","text":"The mammalian cerebral cortex is responsible for higher cognitive functions such as perception, consciousness, and acquiring and processing information. The neocortex is organized into six distinct laminae, each composed of a rich diversity of cell types which assemble into highly complex cortical circuits. Radial glia progenitors (RGPs) are responsible for producing all neocortical neurons and certain glia lineages. Here, we discuss recent discoveries emerging from clonal lineage analysis at the single RGP cell level that provide us with an inaugural quantitative framework of RGP lineage progression. We further discuss the importance of the relative contribution of intrinsic gene functions and non-cell-autonomous or community effects in regulating RGP proliferation behavior and lineage progression."}],"file_date_updated":"2020-07-14T12:47:24Z","department":[{"_id":"SiHi"}],"ddc":["571","610"],"date_updated":"2024-02-14T12:02:08Z","pubrep_id":"928","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc/4.0/legalcode","image":"/images/cc_by_nc.png","name":"Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)","short":"CC BY-NC (4.0)"},"type":"journal_article","_id":"621","date_created":"2018-12-11T11:47:32Z","date_published":"2017-12-01T00:00:00Z","doi":"10.1002/1873-3468.12906","page":"3993 - 4008","publication":"FEBS letters","day":"01","year":"2017","has_accepted_license":"1","oa":1,"quality_controlled":"1","publisher":"Wiley-Blackwell","title":"Mechanisms of radial glia progenitor cell lineage progression","article_processing_charge":"Yes (in subscription journal)","external_id":{"pmid":["29121403"]},"publist_id":"7183","author":[{"orcid":"0000-0002-8483-8753","full_name":"Beattie, Robert J","last_name":"Beattie","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","first_name":"Robert J"},{"orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"ista":"Beattie RJ, Hippenmeyer S. 2017. Mechanisms of radial glia progenitor cell lineage progression. FEBS letters. 591(24), 3993–4008.","chicago":"Beattie, Robert J, and Simon Hippenmeyer. “Mechanisms of Radial Glia Progenitor Cell Lineage Progression.” FEBS Letters. Wiley-Blackwell, 2017. https://doi.org/10.1002/1873-3468.12906.","apa":"Beattie, R. J., & Hippenmeyer, S. (2017). Mechanisms of radial glia progenitor cell lineage progression. FEBS Letters. Wiley-Blackwell. https://doi.org/10.1002/1873-3468.12906","ama":"Beattie RJ, Hippenmeyer S. Mechanisms of radial glia progenitor cell lineage progression. FEBS letters. 2017;591(24):3993-4008. doi:10.1002/1873-3468.12906","short":"R.J. Beattie, S. Hippenmeyer, FEBS Letters 591 (2017) 3993–4008.","ieee":"R. J. Beattie and S. Hippenmeyer, “Mechanisms of radial glia progenitor cell lineage progression,” FEBS letters, vol. 591, no. 24. Wiley-Blackwell, pp. 3993–4008, 2017.","mla":"Beattie, Robert J., and Simon Hippenmeyer. “Mechanisms of Radial Glia Progenitor Cell Lineage Progression.” FEBS Letters, vol. 591, no. 24, Wiley-Blackwell, 2017, pp. 3993–4008, doi:10.1002/1873-3468.12906."},"project":[{"_id":"25D7962E-B435-11E9-9278-68D0E5697425","grant_number":"RGP0053/2014","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level"},{"grant_number":"618444","name":"Molecular Mechanisms of Cerebral Cortex Development","call_identifier":"FP7","_id":"25D61E48-B435-11E9-9278-68D0E5697425"}]},{"oa":1,"publisher":"Frontiers Research Foundation","quality_controlled":"1","year":"2017","has_accepted_license":"1","isi":1,"publication":"Frontiers in Cellular Neuroscience","day":"28","date_created":"2018-12-11T11:49:25Z","date_published":"2017-06-28T00:00:00Z","doi":"10.3389/fncel.2017.00176","article_number":"176","project":[{"call_identifier":"FP7","_id":"25D61E48-B435-11E9-9278-68D0E5697425","name":"Molecular Mechanisms of Cerebral Cortex Development","grant_number":"618444"},{"_id":"25D7962E-B435-11E9-9278-68D0E5697425","grant_number":"RGP0053/2014","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level"},{"grant_number":"291734","name":"International IST Postdoc Fellowship Programme","call_identifier":"FP7","_id":"25681D80-B435-11E9-9278-68D0E5697425"},{"_id":"25985A36-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"T00817-B21","name":"The biochemical basis of PAR polarization"}],"citation":{"apa":"Hansen, A. H., Düllberg, C. F., Mieck, C., Loose, M., & Hippenmeyer, S. (2017). Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks. Frontiers in Cellular Neuroscience. Frontiers Research Foundation. https://doi.org/10.3389/fncel.2017.00176","ama":"Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks. Frontiers in Cellular Neuroscience. 2017;11. doi:10.3389/fncel.2017.00176","ieee":"A. H. Hansen, C. F. Düllberg, C. Mieck, M. Loose, and S. Hippenmeyer, “Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks,” Frontiers in Cellular Neuroscience, vol. 11. Frontiers Research Foundation, 2017.","short":"A.H. Hansen, C.F. Düllberg, C. Mieck, M. Loose, S. Hippenmeyer, Frontiers in Cellular Neuroscience 11 (2017).","mla":"Hansen, Andi H., et al. “Cell Polarity in Cerebral Cortex Development - Cellular Architecture Shaped by Biochemical Networks.” Frontiers in Cellular Neuroscience, vol. 11, 176, Frontiers Research Foundation, 2017, doi:10.3389/fncel.2017.00176.","ista":"Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. 2017. Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks. Frontiers in Cellular Neuroscience. 11, 176.","chicago":"Hansen, Andi H, Christian F Düllberg, Christine Mieck, Martin Loose, and Simon Hippenmeyer. “Cell Polarity in Cerebral Cortex Development - Cellular Architecture Shaped by Biochemical Networks.” Frontiers in Cellular Neuroscience. Frontiers Research Foundation, 2017. https://doi.org/10.3389/fncel.2017.00176."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","external_id":{"isi":["000404486700001"]},"article_processing_charge":"Yes","author":[{"first_name":"Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87","full_name":"Hansen, Andi H","last_name":"Hansen"},{"last_name":"Düllberg","orcid":"0000-0001-6335-9748","full_name":"Düllberg, Christian F","first_name":"Christian F","id":"459064DC-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Mieck, Christine","orcid":"0000-0003-1919-7416","last_name":"Mieck","id":"34CAE85C-F248-11E8-B48F-1D18A9856A87","first_name":"Christine"},{"orcid":"0000-0001-7309-9724","full_name":"Loose, Martin","last_name":"Loose","id":"462D4284-F248-11E8-B48F-1D18A9856A87","first_name":"Martin"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer"}],"publist_id":"6445","title":"Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks","abstract":[{"text":"The human cerebral cortex is the seat of our cognitive abilities and composed of an extraordinary number of neurons, organized in six distinct layers. The establishment of specific morphological and physiological features in individual neurons needs to be regulated with high precision. Impairments in the sequential developmental programs instructing corticogenesis lead to alterations in the cortical cytoarchitecture which is thought to represent the major underlying cause for several neurological disorders including neurodevelopmental and psychiatric diseases. In this review we discuss the role of cell polarity at sequential stages during cortex development. We first provide an overview of morphological cell polarity features in cortical neural stem cells and newly-born postmitotic neurons. We then synthesize a conceptual molecular and biochemical framework how cell polarity is established at the cellular level through a break in symmetry in nascent cortical projection neurons. Lastly we provide a perspective how the molecular mechanisms applying to single cells could be probed and integrated in an in vivo and tissue-wide context.","lang":"eng"}],"oa_version":"Published Version","scopus_import":"1","intvolume":" 11","month":"06","publication_status":"published","publication_identifier":{"issn":["16625102"]},"language":[{"iso":"eng"}],"file":[{"file_id":"4764","checksum":"dc1f5a475b918d09a0f9f587400b1626","access_level":"open_access","relation":"main_file","content_type":"application/pdf","date_created":"2018-12-12T10:09:40Z","file_name":"IST-2017-830-v1+1_2017_Hansen_CellPolarity.pdf","creator":"system","date_updated":"2020-07-14T12:48:16Z","file_size":2153858}],"ec_funded":1,"volume":11,"related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"9962"}]},"_id":"960","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","pubrep_id":"830","status":"public","date_updated":"2024-03-27T23:30:40Z","ddc":["570"],"department":[{"_id":"SiHi"},{"_id":"MaLo"}],"file_date_updated":"2020-07-14T12:48:16Z"},{"date_created":"2018-12-11T11:50:35Z","date_published":"2016-11-09T00:00:00Z","volume":36,"doi":"10.1523/JNEUROSCI.2359-16.2016","issue":"45","page":"11394 - 11401","publication":"Journal of Neuroscience","language":[{"iso":"eng"}],"day":"09","year":"2016","publication_status":"published","intvolume":" 36","month":"11","scopus_import":1,"quality_controlled":"1","publisher":"Society for Neuroscience","acknowledgement":"This work was supported by National Institutes of Health Grants R01NS089795 and R01NS098370 to H.T.G., R01NS076640 to N.D.D., and R01MH094589 and R01NS089777 to B.C., Academia Sinica AS-104-TPB09-2 to S.-J.C, European Union FP7-CIG618444 and Human Frontiers Science Program RGP0053 to S.H., and Fonds Léon Fredericq, from the Fondation Médicale Reine Elisabeth, and from the Fonation Simone et Pierre Clerdent to L.N. The authors apologize to colleagues whose work could not be cited due to space limitations.","oa_version":"None","abstract":[{"lang":"eng","text":"This review accompanies a 2016 SFN mini-symposium presenting examples of current studies that address a central question: How do neural stem cells (NSCs) divide in different ways to produce heterogeneous daughter types at the right time and in proper numbers to build a cerebral cortex with the appropriate size and structure? We will focus on four aspects of corticogenesis: cytokinesis events that follow apical mitoses of NSCs; coordinating abscission with delamination from the apical membrane; timing of neurogenesis and its indirect regulation through emergence of intermediate progenitors; and capacity of single NSCs to generate the correct number and laminar fate of cortical neurons. Defects in these mechanisms can cause microcephaly and other brain malformations, and understanding them is critical to designing diagnostic tools and preventive and corrective therapies."}],"department":[{"_id":"SiHi"}],"title":"Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and productivity","author":[{"last_name":"Dwyer","full_name":"Dwyer, Noelle","first_name":"Noelle"},{"full_name":"Chen, Bin","last_name":"Chen","first_name":"Bin"},{"full_name":"Chou, Shen","last_name":"Chou","first_name":"Shen"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061"},{"last_name":"Nguyen","full_name":"Nguyen, Laurent","first_name":"Laurent"},{"first_name":"Troy","full_name":"Ghashghaei, Troy","last_name":"Ghashghaei"}],"publist_id":"6172","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T06:48:54Z","citation":{"mla":"Dwyer, Noelle, et al. “Neural Stem Cells to Cerebral Cortex: Emerging Mechanisms Regulating Progenitor Behavior and Productivity.” Journal of Neuroscience, vol. 36, no. 45, Society for Neuroscience, 2016, pp. 11394–401, doi:10.1523/JNEUROSCI.2359-16.2016.","apa":"Dwyer, N., Chen, B., Chou, S., Hippenmeyer, S., Nguyen, L., & Ghashghaei, T. (2016). Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and productivity. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.2359-16.2016","ama":"Dwyer N, Chen B, Chou S, Hippenmeyer S, Nguyen L, Ghashghaei T. Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and productivity. Journal of Neuroscience. 2016;36(45):11394-11401. doi:10.1523/JNEUROSCI.2359-16.2016","short":"N. Dwyer, B. Chen, S. Chou, S. Hippenmeyer, L. Nguyen, T. Ghashghaei, Journal of Neuroscience 36 (2016) 11394–11401.","ieee":"N. Dwyer, B. Chen, S. Chou, S. Hippenmeyer, L. Nguyen, and T. Ghashghaei, “Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and productivity,” Journal of Neuroscience, vol. 36, no. 45. Society for Neuroscience, pp. 11394–11401, 2016.","chicago":"Dwyer, Noelle, Bin Chen, Shen Chou, Simon Hippenmeyer, Laurent Nguyen, and Troy Ghashghaei. “Neural Stem Cells to Cerebral Cortex: Emerging Mechanisms Regulating Progenitor Behavior and Productivity.” Journal of Neuroscience. Society for Neuroscience, 2016. https://doi.org/10.1523/JNEUROSCI.2359-16.2016.","ista":"Dwyer N, Chen B, Chou S, Hippenmeyer S, Nguyen L, Ghashghaei T. 2016. Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and productivity. Journal of Neuroscience. 36(45), 11394–11401."},"status":"public","project":[{"grant_number":"RGP0053/2014","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level","_id":"25D7962E-B435-11E9-9278-68D0E5697425"}],"type":"journal_article","_id":"1181"},{"date_updated":"2023-02-23T10:01:08Z","ddc":["570"],"file_date_updated":"2020-07-14T12:44:57Z","department":[{"_id":"SiHi"}],"_id":"1488","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","pubrep_id":"517","status":"public","publication_status":"published","language":[{"iso":"eng"}],"file":[{"date_updated":"2020-07-14T12:44:57Z","file_size":5904773,"creator":"system","date_created":"2018-12-12T10:13:42Z","file_name":"IST-2016-517-v1+1_journal.pbio.1002382_1_.PDF","content_type":"application/pdf","access_level":"open_access","relation":"main_file","checksum":"7f8fa1b3a29f94c0a14dd4465278cdbc","file_id":"5027"}],"volume":14,"related_material":{"record":[{"relation":"research_data","status":"deleted","id":"9703"}]},"issue":"2","abstract":[{"lang":"eng","text":"Branching morphogenesis of the epithelial ureteric bud forms the renal collecting duct system and is critical for normal nephron number, while low nephron number is implicated in hypertension and renal disease. Ureteric bud growth and branching requires GDNF signaling from the surrounding mesenchyme to cells at the ureteric bud tips, via the Ret receptor tyrosine kinase and coreceptor Gfrα1; Ret signaling up-regulates transcription factors Etv4 and Etv5, which are also critical for branching. Despite extensive knowledge of the genetic control of these events, it is not understood, at the cellular level, how renal branching morphogenesis is achieved or how Ret signaling influences epithelial cell behaviors to promote this process. Analysis of chimeric embryos previously suggested a role for Ret signaling in promoting cell rearrangements in the nephric duct, but this method was unsuited to study individual cell behaviors during ureteric bud branching. Here, we use Mosaic Analysis with Double Markers (MADM), combined with organ culture and time-lapse imaging, to trace the movements and divisions of individual ureteric bud tip cells. We first examine wild-type clones and then Ret or Etv4 mutant/wild-type clones in which the mutant and wild-type sister cells are differentially and heritably marked by green and red fluorescent proteins. We find that, in normal kidneys, most individual tip cells behave as self-renewing progenitors, some of whose progeny remain at the tips while others populate the growing UB trunks. In Ret or Etv4 MADM clones, the wild-type cells generated at a UB tip are much more likely to remain at, or move to, the new tips during branching and elongation, while their Ret−/− or Etv4−/− sister cells tend to lag behind and contribute only to the trunks. By tracking successive mitoses in a cell lineage, we find that Ret signaling has little effect on proliferation, in contrast to its effects on cell movement. Our results show that Ret/Etv4 signaling promotes directed cell movements in the ureteric bud tips, and suggest a model in which these cell movements mediate branching morphogenesis."}],"oa_version":"Published Version","scopus_import":1,"intvolume":" 14","month":"02","citation":{"apa":"Riccio, P., Cebrián, C., Zong, H., Hippenmeyer, S., & Costantini, F. (2016). Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis. PLoS Biology. Public Library of Science. https://doi.org/10.1371/journal.pbio.1002382","ama":"Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis. PLoS Biology. 2016;14(2). doi:10.1371/journal.pbio.1002382","short":"P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, F. Costantini, PLoS Biology 14 (2016).","ieee":"P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, and F. Costantini, “Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis,” PLoS Biology, vol. 14, no. 2. Public Library of Science, 2016.","mla":"Riccio, Paul, et al. “Ret and Etv4 Promote Directed Movements of Progenitor Cells during Renal Branching Morphogenesis.” PLoS Biology, vol. 14, no. 2, e1002382, Public Library of Science, 2016, doi:10.1371/journal.pbio.1002382.","ista":"Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. 2016. Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis. PLoS Biology. 14(2), e1002382.","chicago":"Riccio, Paul, Cristina Cebrián, Hui Zong, Simon Hippenmeyer, and Frank Costantini. “Ret and Etv4 Promote Directed Movements of Progenitor Cells during Renal Branching Morphogenesis.” PLoS Biology. Public Library of Science, 2016. https://doi.org/10.1371/journal.pbio.1002382."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publist_id":"5699","author":[{"first_name":"Paul","last_name":"Riccio","full_name":"Riccio, Paul"},{"first_name":"Cristina","last_name":"Cebrián","full_name":"Cebrián, Cristina"},{"first_name":"Hui","last_name":"Zong","full_name":"Zong, Hui"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"},{"last_name":"Costantini","full_name":"Costantini, Frank","first_name":"Frank"}],"title":"Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis","article_number":"e1002382","year":"2016","has_accepted_license":"1","publication":"PLoS Biology","day":"19","date_created":"2018-12-11T11:52:19Z","doi":"10.1371/journal.pbio.1002382","date_published":"2016-02-19T00:00:00Z","acknowledgement":"We thank Silvia Arber, Thomas Jessell, Kenneth M. Murphy, Carlton Bates, Hideki Enomoto, Liqun Luo and Andrew McMahon for mouse strains; Thomas Jessell for antibodies; and Laura Martinez Prat for experimental assistance.","oa":1,"publisher":"Public Library of Science","quality_controlled":"1"},{"date_published":"2015-09-02T00:00:00Z","doi":"10.1016/j.neuron.2015.07.011","date_created":"2018-12-11T11:52:40Z","page":"989 - 998","day":"02","publication":"Neuron","year":"2015","publisher":"Elsevier","quality_controlled":"1","oa":1,"acknowledgement":"Research in the G.F. laboratory is supported by NIH (NS 081297, MH095147, and P01NS074972) and the Simons Foundation. Research in the S.H. laboratory is supported by the European Union (FP7-CIG618444). C.M. is supported by EMBO ALTF (1295-2012). X.H.J. is supported by EMBO (ALTF 303-2010) and HFSP (LT000078/2011-L).\r\n\r\n","title":"Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries","author":[{"first_name":"Christian","full_name":"Mayer, Christian","last_name":"Mayer"},{"first_name":"Xavier","full_name":"Jaglin, Xavier","last_name":"Jaglin"},{"full_name":"Cobbs, Lucy","last_name":"Cobbs","first_name":"Lucy"},{"last_name":"Bandler","full_name":"Bandler, Rachel","first_name":"Rachel"},{"first_name":"Carmen","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","full_name":"Streicher, Carmen","last_name":"Streicher"},{"full_name":"Cepko, Constance","last_name":"Cepko","first_name":"Constance"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer"},{"first_name":"Gord","last_name":"Fishell","full_name":"Fishell, Gord"}],"publist_id":"5621","external_id":{"pmid":["26299473"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Mayer, Christian, Xavier Jaglin, Lucy Cobbs, Rachel Bandler, Carmen Streicher, Constance Cepko, Simon Hippenmeyer, and Gord Fishell. “Clonally Related Forebrain Interneurons Disperse Broadly across Both Functional Areas and Structural Boundaries.” Neuron. Elsevier, 2015. https://doi.org/10.1016/j.neuron.2015.07.011.","ista":"Mayer C, Jaglin X, Cobbs L, Bandler R, Streicher C, Cepko C, Hippenmeyer S, Fishell G. 2015. Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries. Neuron. 87(5), 989–998.","mla":"Mayer, Christian, et al. “Clonally Related Forebrain Interneurons Disperse Broadly across Both Functional Areas and Structural Boundaries.” Neuron, vol. 87, no. 5, Elsevier, 2015, pp. 989–98, doi:10.1016/j.neuron.2015.07.011.","ieee":"C. Mayer et al., “Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries,” Neuron, vol. 87, no. 5. Elsevier, pp. 989–998, 2015.","short":"C. Mayer, X. Jaglin, L. Cobbs, R. Bandler, C. Streicher, C. Cepko, S. Hippenmeyer, G. Fishell, Neuron 87 (2015) 989–998.","apa":"Mayer, C., Jaglin, X., Cobbs, L., Bandler, R., Streicher, C., Cepko, C., … Fishell, G. (2015). Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2015.07.011","ama":"Mayer C, Jaglin X, Cobbs L, et al. Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries. Neuron. 2015;87(5):989-998. doi:10.1016/j.neuron.2015.07.011"},"volume":87,"issue":"5","language":[{"iso":"eng"}],"publication_status":"published","month":"09","intvolume":" 87","scopus_import":1,"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4560602/"}],"pmid":1,"oa_version":"Submitted Version","abstract":[{"text":"The medial ganglionic eminence (MGE) gives rise to the majority of mouse forebrain interneurons. Here, we examine the lineage relationship among MGE-derived interneurons using a replication-defective retroviral library containing a highly diverse set of DNA barcodes. Recovering the barcodes from the mature progeny of infected progenitor cells enabled us to unambiguously determine their respective lineal relationship. We found that clonal dispersion occurs across large areas of the brain and is not restricted by anatomical divisions. As such, sibling interneurons can populate the cortex, hippocampus striatum, and globus pallidus. The majority of interneurons appeared to be generated from asymmetric divisions of MGE progenitor cells, followed by symmetric divisions within the subventricular zone. Altogether, our findings uncover that lineage relationships do not appear to determine interneuron allocation to particular regions. As such, it is likely that clonally related interneurons have considerable flexibility as to the particular forebrain circuits to which they can contribute.","lang":"eng"}],"department":[{"_id":"SiHi"}],"date_updated":"2021-01-12T06:51:32Z","status":"public","type":"journal_article","_id":"1550"},{"publication":"Nature Cell Biology","day":"13","year":"2014","date_created":"2018-12-11T11:54:36Z","date_published":"2014-07-13T00:00:00Z","doi":"10.1038/ncb3001","page":"758 - 769","oa":1,"quality_controlled":"1","publisher":"Nature Publishing Group","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"ista":"Williams S, Ratliff L, Postiglione MP, Knoblich J, Fuchs E. 2014. Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. Nature Cell Biology. 16(8), 758–769.","chicago":"Williams, Scott, Lyndsay Ratliff, Maria P Postiglione, Juergen Knoblich, and Elaine Fuchs. “Par3-MInsc and Gα I3 Cooperate to Promote Oriented Epidermal Cell Divisions through LGN.” Nature Cell Biology. Nature Publishing Group, 2014. https://doi.org/10.1038/ncb3001.","ama":"Williams S, Ratliff L, Postiglione MP, Knoblich J, Fuchs E. Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. Nature Cell Biology. 2014;16(8):758-769. doi:10.1038/ncb3001","apa":"Williams, S., Ratliff, L., Postiglione, M. P., Knoblich, J., & Fuchs, E. (2014). Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb3001","ieee":"S. Williams, L. Ratliff, M. P. Postiglione, J. Knoblich, and E. Fuchs, “Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN,” Nature Cell Biology, vol. 16, no. 8. Nature Publishing Group, pp. 758–769, 2014.","short":"S. Williams, L. Ratliff, M.P. Postiglione, J. Knoblich, E. Fuchs, Nature Cell Biology 16 (2014) 758–769.","mla":"Williams, Scott, et al. “Par3-MInsc and Gα I3 Cooperate to Promote Oriented Epidermal Cell Divisions through LGN.” Nature Cell Biology, vol. 16, no. 8, Nature Publishing Group, 2014, pp. 758–69, doi:10.1038/ncb3001."},"title":"Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN","article_processing_charge":"No","external_id":{"pmid":["25016959"]},"publist_id":"5196","author":[{"full_name":"Williams, Scott","last_name":"Williams","first_name":"Scott"},{"first_name":"Lyndsay","full_name":"Ratliff, Lyndsay","last_name":"Ratliff"},{"first_name":"Maria P","id":"2C67902A-F248-11E8-B48F-1D18A9856A87","full_name":"Postiglione, Maria P","last_name":"Postiglione"},{"last_name":"Knoblich","full_name":"Knoblich, Juergen","first_name":"Juergen"},{"first_name":"Elaine","full_name":"Fuchs, Elaine","last_name":"Fuchs"}],"language":[{"iso":"eng"}],"publication_status":"published","volume":16,"issue":"8","oa_version":"Submitted Version","pmid":1,"abstract":[{"lang":"eng","text":"Asymmetric cell divisions allow stem cells to balance proliferation and differentiation. During embryogenesis, murine epidermis expands rapidly from a single layer of unspecified basal layer progenitors to a stratified, differentiated epithelium. Morphogenesis involves perpendicular (asymmetric) divisions and the spindle orientation protein LGN, but little is known about how the apical localization of LGN is regulated. Here, we combine conventional genetics and lentiviral-mediated in vivo RNAi to explore the functions of the LGN-interacting proteins Par3, mInsc and Gα i3. Whereas loss of each gene alone leads to randomized division angles, combined loss of Gnai3 and mInsc causes a phenotype of mostly planar divisions, akin to loss of LGN. These findings lend experimental support for the hitherto untested model that Par3-mInsc and Gα i3 act cooperatively to polarize LGN and promote perpendicular divisions. Finally, we uncover a developmental switch between delamination-driven early stratification and spindle-orientation-dependent differentiation that occurs around E15, revealing a two-step mechanism underlying epidermal maturation."}],"intvolume":" 16","month":"07","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159251/"}],"scopus_import":1,"date_updated":"2021-01-12T06:53:55Z","department":[{"_id":"SiHi"}],"_id":"1899","status":"public","article_type":"original","type":"journal_article"},{"scopus_import":1,"intvolume":" 159","month":"11","abstract":[{"text":"Radial glial progenitors (RGPs) are responsible for producing nearly all neocortical neurons. To gain insight into the patterns of RGP division and neuron production, we quantitatively analyzed excitatory neuron genesis in the mouse neocortex using Mosaic Analysis with Double Markers, which provides single-cell resolution of progenitor division patterns and potential in vivo. We found that RGPs progress through a coherent program in which their proliferative potential diminishes in a predictable manner. Upon entry into the neurogenic phase, individual RGPs produce ∼8–9 neurons distributed in both deep and superficial layers, indicating a unitary output in neuronal production. Removal of OTX1, a transcription factor transiently expressed in RGPs, results in both deep- and superficial-layer neuron loss and a reduction in neuronal unit size. Moreover, ∼1/6 of neurogenic RGPs proceed to produce glia. These results suggest that progenitor behavior and histogenesis in the mammalian neocortex conform to a remarkably orderly and deterministic program.","lang":"eng"}],"oa_version":"Published Version","ec_funded":1,"issue":"4","volume":159,"publication_status":"published","language":[{"iso":"eng"}],"file":[{"checksum":"6c5de8329bb2ffa71cba9fda750f14ce","file_id":"4709","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"IST-2016-423-v1+1_1-s2.0-S0092867414013154-main.pdf","date_created":"2018-12-12T10:08:47Z","creator":"system","file_size":4435787,"date_updated":"2020-07-14T12:45:25Z"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","pubrep_id":"423","status":"public","_id":"2022","file_date_updated":"2020-07-14T12:45:25Z","department":[{"_id":"SiHi"},{"_id":"Bio"}],"date_updated":"2021-01-12T06:54:47Z","ddc":["570"],"oa":1,"publisher":"Cell Press","quality_controlled":"1","page":"775 - 788","date_created":"2018-12-11T11:55:16Z","date_published":"2014-11-06T00:00:00Z","doi":"10.1016/j.cell.2014.10.027","year":"2014","has_accepted_license":"1","publication":"Cell","day":"06","project":[{"grant_number":"618444","name":"Molecular Mechanisms of Cerebral Cortex Development","call_identifier":"FP7","_id":"25D61E48-B435-11E9-9278-68D0E5697425"},{"_id":"25D7962E-B435-11E9-9278-68D0E5697425","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level","grant_number":"RGP0053/2014"}],"author":[{"first_name":"Peng","last_name":"Gao","full_name":"Gao, Peng"},{"id":"2C67902A-F248-11E8-B48F-1D18A9856A87","first_name":"Maria P","last_name":"Postiglione","full_name":"Postiglione, Maria P"},{"full_name":"Krieger, Teresa","last_name":"Krieger","first_name":"Teresa"},{"first_name":"Luisirene","last_name":"Hernandez","full_name":"Hernandez, Luisirene"},{"first_name":"Chao","full_name":"Wang, Chao","last_name":"Wang"},{"first_name":"Zhi","full_name":"Han, Zhi","last_name":"Han"},{"first_name":"Carmen","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","last_name":"Streicher","full_name":"Streicher, Carmen"},{"first_name":"Ekaterina","id":"41DB591E-F248-11E8-B48F-1D18A9856A87","full_name":"Papusheva, Ekaterina","last_name":"Papusheva"},{"first_name":"Ryan","full_name":"Insolera, Ryan","last_name":"Insolera"},{"first_name":"Kritika","full_name":"Chugh, Kritika","last_name":"Chugh"},{"last_name":"Kodish","full_name":"Kodish, Oren","first_name":"Oren"},{"full_name":"Huang, Kun","last_name":"Huang","first_name":"Kun"},{"first_name":"Benjamin","full_name":"Simons, Benjamin","last_name":"Simons"},{"last_name":"Luo","full_name":"Luo, Liqun","first_name":"Liqun"},{"orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Shi","full_name":"Shi, Song","first_name":"Song"}],"publist_id":"5050","title":"Deterministic progenitor behavior and unitary production of neurons in the neocortex","citation":{"mla":"Gao, Peng, et al. “Deterministic Progenitor Behavior and Unitary Production of Neurons in the Neocortex.” Cell, vol. 159, no. 4, Cell Press, 2014, pp. 775–88, doi:10.1016/j.cell.2014.10.027.","ieee":"P. Gao et al., “Deterministic progenitor behavior and unitary production of neurons in the neocortex,” Cell, vol. 159, no. 4. Cell Press, pp. 775–788, 2014.","short":"P. Gao, M.P. Postiglione, T. Krieger, L. Hernandez, C. Wang, Z. Han, C. Streicher, E. Papusheva, R. Insolera, K. Chugh, O. Kodish, K. Huang, B. Simons, L. Luo, S. Hippenmeyer, S. Shi, Cell 159 (2014) 775–788.","ama":"Gao P, Postiglione MP, Krieger T, et al. Deterministic progenitor behavior and unitary production of neurons in the neocortex. Cell. 2014;159(4):775-788. doi:10.1016/j.cell.2014.10.027","apa":"Gao, P., Postiglione, M. P., Krieger, T., Hernandez, L., Wang, C., Han, Z., … Shi, S. (2014). Deterministic progenitor behavior and unitary production of neurons in the neocortex. Cell. Cell Press. https://doi.org/10.1016/j.cell.2014.10.027","chicago":"Gao, Peng, Maria P Postiglione, Teresa Krieger, Luisirene Hernandez, Chao Wang, Zhi Han, Carmen Streicher, et al. “Deterministic Progenitor Behavior and Unitary Production of Neurons in the Neocortex.” Cell. Cell Press, 2014. https://doi.org/10.1016/j.cell.2014.10.027.","ista":"Gao P, Postiglione MP, Krieger T, Hernandez L, Wang C, Han Z, Streicher C, Papusheva E, Insolera R, Chugh K, Kodish O, Huang K, Simons B, Luo L, Hippenmeyer S, Shi S. 2014. Deterministic progenitor behavior and unitary production of neurons in the neocortex. Cell. 159(4), 775–788."},"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87"},{"language":[{"iso":"eng"}],"publication":"PNAS","day":"17","year":"2014","publication_status":"published","date_created":"2018-12-11T11:55:15Z","date_published":"2014-06-17T00:00:00Z","issue":"24","volume":111,"doi":"10.1073/pnas.1408233111","page":"8850 - 8855","oa_version":"None","abstract":[{"lang":"eng","text":"The mammalian heart has long been considered a postmitotic organ, implying that the total number of cardiomyocytes is set at birth. Analysis of cell division in the mammalian heart is complicated by cardiomyocyte binucleation shortly after birth, which makes it challenging to interpret traditional assays of cell turnover [Laflamme MA, Murray CE (2011) Nature 473(7347):326–335; Bergmann O, et al. (2009) Science 324(5923):98–102]. An elegant multi-isotope imaging-mass spectrometry technique recently calculated the low, discrete rate of cardiomyocyte generation in mice [Senyo SE, et al. (2013) Nature 493(7432):433–436], yet our cellular-level understanding of postnatal cardiomyogenesis remains limited. Herein, we provide a new line of evidence for the differentiated α-myosin heavy chain-expressing cardiomyocyte as the cell of origin of postnatal cardiomyogenesis using the “mosaic analysis with double markers” mouse model. We show limited, life-long, symmetric division of cardiomyocytes as a rare event that is evident in utero but significantly diminishes after the first month of life in mice; daughter cardiomyocytes divide very seldom, which this study is the first to demonstrate, to our knowledge. Furthermore, ligation of the left anterior descending coronary artery, which causes a myocardial infarction in the mosaic analysis with double-marker mice, did not increase the rate of cardiomyocyte division above the basal level for up to 4 wk after the injury. The clonal analysis described here provides direct evidence of postnatal mammalian cardiomyogenesis."}],"intvolume":" 111","month":"06","publisher":"National Academy of Sciences","scopus_import":1,"quality_controlled":"1","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","citation":{"apa":"Ali, S., Hippenmeyer, S., Saadat, L., Luo, L., Weissman, I., & Ardehali, R. (2014). Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1408233111","ama":"Ali S, Hippenmeyer S, Saadat L, Luo L, Weissman I, Ardehali R. Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice. PNAS. 2014;111(24):8850-8855. doi:10.1073/pnas.1408233111","short":"S. Ali, S. Hippenmeyer, L. Saadat, L. Luo, I. Weissman, R. Ardehali, PNAS 111 (2014) 8850–8855.","ieee":"S. Ali, S. Hippenmeyer, L. Saadat, L. Luo, I. Weissman, and R. Ardehali, “Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice,” PNAS, vol. 111, no. 24. National Academy of Sciences, pp. 8850–8855, 2014.","mla":"Ali, Shah, et al. “Existing Cardiomyocytes Generate Cardiomyocytes at a Low Rate after Birth in Mice.” PNAS, vol. 111, no. 24, National Academy of Sciences, 2014, pp. 8850–55, doi:10.1073/pnas.1408233111.","ista":"Ali S, Hippenmeyer S, Saadat L, Luo L, Weissman I, Ardehali R. 2014. Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice. PNAS. 111(24), 8850–8855.","chicago":"Ali, Shah, Simon Hippenmeyer, Lily Saadat, Liqun Luo, Irving Weissman, and Reza Ardehali. “Existing Cardiomyocytes Generate Cardiomyocytes at a Low Rate after Birth in Mice.” PNAS. National Academy of Sciences, 2014. https://doi.org/10.1073/pnas.1408233111."},"date_updated":"2021-01-12T06:54:46Z","department":[{"_id":"SiHi"}],"title":"Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice","publist_id":"5052","author":[{"full_name":"Ali, Shah","last_name":"Ali","first_name":"Shah"},{"last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"},{"first_name":"Lily","last_name":"Saadat","full_name":"Saadat, Lily"},{"first_name":"Liqun","full_name":"Luo, Liqun","last_name":"Luo"},{"first_name":"Irving","full_name":"Weissman, Irving","last_name":"Weissman"},{"first_name":"Reza","full_name":"Ardehali, Reza","last_name":"Ardehali"}],"_id":"2020","status":"public","type":"journal_article"},{"_id":"2021","status":"public","type":"journal_article","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"William, Joo, Simon Hippenmeyer, and Liqun Luo. “Dendrite Morphogenesis Depends on Relative Levels of NT-3/TrkC Signaling.” Science. American Association for the Advancement of Science, 2014. https://doi.org/10.1126/science.1258996.","ista":"William J, Hippenmeyer S, Luo L. 2014. Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling. Science. 346(6209), 626–629.","mla":"William, Joo, et al. “Dendrite Morphogenesis Depends on Relative Levels of NT-3/TrkC Signaling.” Science, vol. 346, no. 6209, American Association for the Advancement of Science, 2014, pp. 626–29, doi:10.1126/science.1258996.","apa":"William, J., Hippenmeyer, S., & Luo, L. (2014). Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.1258996","ama":"William J, Hippenmeyer S, Luo L. Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling. Science. 2014;346(6209):626-629. doi:10.1126/science.1258996","short":"J. William, S. Hippenmeyer, L. Luo, Science 346 (2014) 626–629.","ieee":"J. William, S. Hippenmeyer, and L. Luo, “Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling,” Science, vol. 346, no. 6209. American Association for the Advancement of Science, pp. 626–629, 2014."},"date_updated":"2021-01-12T06:54:47Z","department":[{"_id":"SiHi"}],"title":"Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling","author":[{"first_name":"Joo","full_name":"William, Joo","last_name":"William"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon"},{"full_name":"Luo, Liqun","last_name":"Luo","first_name":"Liqun"}],"publist_id":"5051","oa_version":"Submitted Version","abstract":[{"lang":"eng","text":"Neurotrophins regulate diverse aspects of neuronal development and plasticity, but their precise in vivo functions during neural circuit assembly in the central brain remain unclear. We show that the neurotrophin receptor tropomyosin-related kinase C (TrkC) is required for dendritic growth and branching of mouse cerebellar Purkinje cells. Sparse TrkC knockout reduced dendrite complexity, but global Purkinje cell knockout had no effect. Removal of the TrkC ligand neurotrophin-3 (NT-3) from cerebellar granule cells, which provide major afferent input to developing Purkinje cell dendrites, rescued the dendrite defects caused by sparse TrkC disruption in Purkinje cells. Our data demonstrate that NT-3 from presynaptic neurons (granule cells) is required for TrkC-dependent competitive dendrite morphogenesis in postsynaptic neurons (Purkinje cells)—a previously unknown mechanism of neural circuit development."}],"month":"10","intvolume":" 346","quality_controlled":"1","publisher":"American Association for the Advancement of Science","scopus_import":1,"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631524/"}],"oa":1,"day":"31","language":[{"iso":"eng"}],"publication":"Science","publication_status":"published","year":"2014","doi":"10.1126/science.1258996","date_published":"2014-10-31T00:00:00Z","volume":346,"issue":"6209","date_created":"2018-12-11T11:55:15Z","page":"626 - 629"},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Zhu, Fangfang, et al. “DICE, an Efficient System for Iterative Genomic Editing in Human Pluripotent Stem Cells.” Nucleic Acids Research, vol. 42, no. 5, e34, Oxford University Press, 2014, doi:10.1093/nar/gkt1290.","short":"F. Zhu, M. Gamboa, A. Farruggio, S. Hippenmeyer, B. Tasic, B. Schüle, Y. Chen Tsai, M. Calos, Nucleic Acids Research 42 (2014).","ieee":"F. Zhu et al., “DICE, an efficient system for iterative genomic editing in human pluripotent stem cells,” Nucleic Acids Research, vol. 42, no. 5. Oxford University Press, 2014.","ama":"Zhu F, Gamboa M, Farruggio A, et al. DICE, an efficient system for iterative genomic editing in human pluripotent stem cells. Nucleic Acids Research. 2014;42(5). doi:10.1093/nar/gkt1290","apa":"Zhu, F., Gamboa, M., Farruggio, A., Hippenmeyer, S., Tasic, B., Schüle, B., … Calos, M. (2014). DICE, an efficient system for iterative genomic editing in human pluripotent stem cells. Nucleic Acids Research. Oxford University Press. https://doi.org/10.1093/nar/gkt1290","chicago":"Zhu, Fangfang, Matthew Gamboa, Alfonso Farruggio, Simon Hippenmeyer, Bosiljka Tasic, Birgitt Schüle, Yanru Chen Tsai, and Michele Calos. “DICE, an Efficient System for Iterative Genomic Editing in Human Pluripotent Stem Cells.” Nucleic Acids Research. Oxford University Press, 2014. https://doi.org/10.1093/nar/gkt1290.","ista":"Zhu F, Gamboa M, Farruggio A, Hippenmeyer S, Tasic B, Schüle B, Chen Tsai Y, Calos M. 2014. DICE, an efficient system for iterative genomic editing in human pluripotent stem cells. Nucleic Acids Research. 42(5), e34."},"title":"DICE, an efficient system for iterative genomic editing in human pluripotent stem cells","publist_id":"4684","author":[{"first_name":"Fangfang","full_name":"Zhu, Fangfang","last_name":"Zhu"},{"last_name":"Gamboa","full_name":"Gamboa, Matthew","first_name":"Matthew"},{"first_name":"Alfonso","last_name":"Farruggio","full_name":"Farruggio, Alfonso"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon"},{"first_name":"Bosiljka","last_name":"Tasic","full_name":"Tasic, Bosiljka"},{"first_name":"Birgitt","full_name":"Schüle, Birgitt","last_name":"Schüle"},{"first_name":"Yanru","full_name":"Chen Tsai, Yanru","last_name":"Chen Tsai"},{"last_name":"Calos","full_name":"Calos, Michele","first_name":"Michele"}],"article_number":"e34","publication":"Nucleic Acids Research","day":"05","year":"2014","has_accepted_license":"1","date_created":"2018-12-11T11:56:38Z","date_published":"2014-03-05T00:00:00Z","doi":"10.1093/nar/gkt1290","acknowledgement":"California Institute for Regenerative Medicine [RT2-01880 and TR2-01756]. Funding for open access charge: California Institute for Regenerative Medicine [RT2-01880 and TR2-01756]\r\nCC BY 3,0","oa":1,"quality_controlled":"1","publisher":"Oxford University Press","ddc":["571","610"],"date_updated":"2021-01-12T06:56:22Z","department":[{"_id":"SiHi"}],"file_date_updated":"2020-07-14T12:45:35Z","_id":"2261","pubrep_id":"961","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","language":[{"iso":"eng"}],"file":[{"file_size":11044478,"date_updated":"2020-07-14T12:45:35Z","creator":"system","file_name":"IST-2018-961-v1+1_2014_Hippenmeyer_DICE.pdf","date_created":"2018-12-12T10:09:15Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_id":"4738","checksum":"e9268f5f96a820f04d7ebbf85927c3cb"}],"publication_status":"published","volume":42,"issue":"5","oa_version":"Preprint","abstract":[{"text":"To reveal the full potential of human pluripotent stem cells, new methods for rapid, site-specific genomic engineering are needed. Here, we describe a system for precise genetic modification of human embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs). We identified a novel human locus, H11, located in a safe, intergenic, transcriptionally active region of chromosome 22, as the recipient site, to provide robust, ubiquitous expression of inserted genes. Recipient cell lines were established by site-specific placement of a ‘landing pad’ cassette carrying attP sites for phiC31 and Bxb1 integrases at the H11 locus by spontaneous or TALEN-assisted homologous recombination. Dual integrase cassette exchange (DICE) mediated by phiC31 and Bxb1 integrases was used to insert genes of interest flanked by phiC31 and Bxb1 attB sites at the H11 locus, replacing the landing pad. This system provided complete control over content, direction and copy number of inserted genes, with a specificity of 100%. A series of genes, including mCherry and various combinations of the neural transcription factors LMX1a, FOXA2 and OTX2, were inserted in recipient cell lines derived from H9 ESC, as well as iPSC lines derived from a Parkinson’s disease patient and a normal sibling control. The DICE system offers rapid, efficient and precise gene insertion in ESC and iPSC and is particularly well suited for repeated modifications of the same locus.","lang":"eng"}],"intvolume":" 42","month":"03","scopus_import":1},{"_id":"2265","status":"public","type":"book_chapter","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Hippenmeyer, Simon. “Molecular Pathways Controlling the Sequential Steps of Cortical Projection Neuron Migration.” In Cellular and Molecular Control of Neuronal Migration, edited by Laurent Nguyen, 800:1–24. Springer, 2014. https://doi.org/10.1007/978-94-007-7687-6_1.","ista":"Hippenmeyer S. 2014.Molecular pathways controlling the sequential steps of cortical projection neuron migration. In: Cellular and Molecular Control of Neuronal Migration. Advances in Experimental Medicine and Biology, vol. 800, 1–24.","mla":"Hippenmeyer, Simon. “Molecular Pathways Controlling the Sequential Steps of Cortical Projection Neuron Migration.” Cellular and Molecular Control of Neuronal Migration, edited by Laurent Nguyen, vol. 800, Springer, 2014, pp. 1–24, doi:10.1007/978-94-007-7687-6_1.","ama":"Hippenmeyer S. Molecular pathways controlling the sequential steps of cortical projection neuron migration. In: Nguyen L, ed. Cellular and Molecular Control of Neuronal Migration. Vol 800. Springer; 2014:1-24. doi:10.1007/978-94-007-7687-6_1","apa":"Hippenmeyer, S. (2014). Molecular pathways controlling the sequential steps of cortical projection neuron migration. In L. Nguyen (Ed.), Cellular and Molecular Control of Neuronal Migration (Vol. 800, pp. 1–24). Springer. https://doi.org/10.1007/978-94-007-7687-6_1","short":"S. Hippenmeyer, in:, L. Nguyen (Ed.), Cellular and Molecular Control of Neuronal Migration, Springer, 2014, pp. 1–24.","ieee":"S. Hippenmeyer, “Molecular pathways controlling the sequential steps of cortical projection neuron migration,” in Cellular and Molecular Control of Neuronal Migration, vol. 800, L. Nguyen, Ed. Springer, 2014, pp. 1–24."},"date_updated":"2021-01-12T06:56:23Z","editor":[{"full_name":"Nguyen, Laurent","last_name":"Nguyen","first_name":"Laurent"}],"title":"Molecular pathways controlling the sequential steps of cortical projection neuron migration","department":[{"_id":"SiHi"}],"author":[{"last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"publist_id":"4679","oa_version":"None","abstract":[{"text":"Coordinated migration of newly-born neurons to their target territories is essential for correct neuronal circuit assembly in the developing brain. Although a cohort of signaling pathways has been implicated in the regulation of cortical projection neuron migration, the precise molecular mechanisms and how a balanced interplay of cell-autonomous and non-autonomous functions of candidate signaling molecules controls the discrete steps in the migration process, are just being revealed. In this chapter, I will focally review recent advances that improved our understanding of the cell-autonomous and possible cell-nonautonomous functions of the evolutionarily conserved LIS1/NDEL1-complex in regulating the sequential steps of cortical projection neuron migration. I will then elaborate on the emerging concept that the Reelin signaling pathway, acts exactly at precise stages in the course of cortical projection neuron migration. Lastly, I will discuss how finely tuned transcriptional programs and downstream effectors govern particular aspects in driving radial migration at discrete stages and how they regulate the precise positioning of cortical projection neurons in the developing cerebral cortex.","lang":"eng"}],"intvolume":" 800","month":"01","scopus_import":1,"quality_controlled":"1","alternative_title":["Advances in Experimental Medicine and Biology"],"publisher":"Springer","publication":" Cellular and Molecular Control of Neuronal Migration","language":[{"iso":"eng"}],"day":"01","publication_status":"published","year":"2014","date_created":"2018-12-11T11:56:39Z","doi":"10.1007/978-94-007-7687-6_1","volume":800,"date_published":"2014-01-01T00:00:00Z","page":"1 - 24"},{"project":[{"grant_number":"618444","name":"Molecular Mechanisms of Cerebral Cortex Development","call_identifier":"FP7","_id":"25D61E48-B435-11E9-9278-68D0E5697425"}],"author":[{"last_name":"Postiglione","full_name":"Postiglione, Maria P","first_name":"Maria P","id":"2C67902A-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"}],"publist_id":"4806","article_processing_charge":"No","title":"Monitoring neurogenesis in the cerebral cortex: an update","citation":{"mla":"Postiglione, Maria P., and Simon Hippenmeyer. “Monitoring Neurogenesis in the Cerebral Cortex: An Update.” Future Neurology, vol. 9, no. 3, Future Science Group, 2014, pp. 323–40, doi:10.2217/fnl.14.18.","short":"M.P. Postiglione, S. Hippenmeyer, Future Neurology 9 (2014) 323–340.","ieee":"M. P. Postiglione and S. Hippenmeyer, “Monitoring neurogenesis in the cerebral cortex: an update,” Future Neurology, vol. 9, no. 3. Future Science Group, pp. 323–340, 2014.","apa":"Postiglione, M. P., & Hippenmeyer, S. (2014). Monitoring neurogenesis in the cerebral cortex: an update. Future Neurology. Future Science Group. https://doi.org/10.2217/fnl.14.18","ama":"Postiglione MP, Hippenmeyer S. Monitoring neurogenesis in the cerebral cortex: an update. Future Neurology. 2014;9(3):323-340. doi:10.2217/fnl.14.18","chicago":"Postiglione, Maria P, and Simon Hippenmeyer. “Monitoring Neurogenesis in the Cerebral Cortex: An Update.” Future Neurology. Future Science Group, 2014. https://doi.org/10.2217/fnl.14.18.","ista":"Postiglione MP, Hippenmeyer S. 2014. Monitoring neurogenesis in the cerebral cortex: an update. Future Neurology. 9(3), 323–340."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","quality_controlled":"1","publisher":"Future Science Group","oa":1,"page":"323 - 340","date_published":"2014-05-01T00:00:00Z","doi":"10.2217/fnl.14.18","date_created":"2018-12-11T11:56:09Z","has_accepted_license":"1","year":"2014","day":"01","publication":"Future Neurology","type":"journal_article","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"status":"public","pubrep_id":"528","_id":"2175","file_date_updated":"2020-07-14T12:45:31Z","department":[{"_id":"SiHi"}],"date_updated":"2023-10-17T08:34:27Z","ddc":["570"],"scopus_import":"1","month":"05","intvolume":" 9","abstract":[{"text":"The cerebral cortex, the seat of our cognitive abilities, is composed of an intricate network of billions of excitatory projection and inhibitory interneurons. Postmitotic cortical neurons are generated by a diverse set of neural stem cell progenitors within dedicated zones and defined periods of neurogenesis during embryonic development. Disruptions in neurogenesis can lead to alterations in the neuronal cytoarchitecture, which is thought to represent a major underlying cause for several neurological disorders, including microcephaly, autism and epilepsy. Although a number of signaling pathways regulating neurogenesis have been described, the precise cellular and molecular mechanisms regulating the functional neural stem cell properties in cortical neurogenesis remain unclear. Here, we discuss the most up-to-date strategies to monitor the fundamental mechanistic parameters of neuronal progenitor proliferation, and recent advances deciphering the logic and dynamics of neurogenesis.","lang":"eng"}],"oa_version":"Published Version","volume":9,"issue":"3","ec_funded":1,"publication_identifier":{"eissn":["1748-6971"],"issn":["1479-6708"]},"publication_status":"published","file":[{"checksum":"ba06659ecadabceec9a37dd8c4586dce","file_id":"4812","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_name":"IST-2016-528-v1+1_fnl.14.18.pdf","date_created":"2018-12-12T10:10:25Z","file_size":3848424,"date_updated":"2020-07-14T12:45:31Z","creator":"system"}],"language":[{"iso":"eng"}]},{"status":"public","type":"journal_article","_id":"2264","department":[{"_id":"SiHi"}],"date_updated":"2021-01-12T06:56:23Z","month":"02","intvolume":" 140","scopus_import":1,"main_file_link":[{"url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561788/","open_access":"1"}],"pmid":1,"oa_version":"Submitted Version","abstract":[{"text":"Faithful progression through the cell cycle is crucial to the maintenance and developmental potential of stem cells. Here, we demonstrate that neural stem cells (NSCs) and intermediate neural progenitor cells (NPCs) employ a zinc-finger transcription factor specificity protein 2 (Sp2) as a cell cycle regulator in two temporally and spatially distinct progenitor domains. Differential conditional deletion of Sp2 in early embryonic cerebral cortical progenitors, and perinatal olfactory bulb progenitors disrupted transitions through G1, G2 and M phases, whereas DNA synthesis appeared intact. Cell-autonomous function of Sp2 was identified by deletion of Sp2 using mosaic analysis with double markers, which clearly established that conditional Sp2-null NSCs and NPCs are M phase arrested in vivo. Importantly, conditional deletion of Sp2 led to a decline in the generation of NPCs and neurons in the developing and postnatal brains. Our findings implicate Sp2-dependent mechanisms as novel regulators of cell cycle progression, the absence of which disrupts neurogenesis in the embryonic and postnatal brain.","lang":"eng"}],"issue":"3","volume":140,"language":[{"iso":"eng"}],"publication_status":"published","title":"Neural development is dependent on the function of specificity protein 2 in cell cycle progression","publist_id":"4681","author":[{"full_name":"Liang, Huixuan","last_name":"Liang","first_name":"Huixuan"},{"first_name":"Guanxi","full_name":"Xiao, Guanxi","last_name":"Xiao"},{"full_name":"Yin, Haifeng","last_name":"Yin","first_name":"Haifeng"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon"},{"last_name":"Horowitz","full_name":"Horowitz, Jonathan","first_name":"Jonathan"},{"last_name":"Ghashghaei","full_name":"Ghashghaei, Troy","first_name":"Troy"}],"article_processing_charge":"No","external_id":{"pmid":["23293287"]},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Liang, Huixuan, et al. “Neural Development Is Dependent on the Function of Specificity Protein 2 in Cell Cycle Progression.” Development, vol. 140, no. 3, Company of Biologists, 2013, pp. 552–61, doi:10.1242/dev.085621.","ama":"Liang H, Xiao G, Yin H, Hippenmeyer S, Horowitz J, Ghashghaei T. Neural development is dependent on the function of specificity protein 2 in cell cycle progression. Development. 2013;140(3):552-561. doi:10.1242/dev.085621","apa":"Liang, H., Xiao, G., Yin, H., Hippenmeyer, S., Horowitz, J., & Ghashghaei, T. (2013). Neural development is dependent on the function of specificity protein 2 in cell cycle progression. Development. Company of Biologists. https://doi.org/10.1242/dev.085621","short":"H. Liang, G. Xiao, H. Yin, S. Hippenmeyer, J. Horowitz, T. Ghashghaei, Development 140 (2013) 552–561.","ieee":"H. Liang, G. Xiao, H. Yin, S. Hippenmeyer, J. Horowitz, and T. Ghashghaei, “Neural development is dependent on the function of specificity protein 2 in cell cycle progression,” Development, vol. 140, no. 3. Company of Biologists, pp. 552–561, 2013.","chicago":"Liang, Huixuan, Guanxi Xiao, Haifeng Yin, Simon Hippenmeyer, Jonathan Horowitz, and Troy Ghashghaei. “Neural Development Is Dependent on the Function of Specificity Protein 2 in Cell Cycle Progression.” Development. Company of Biologists, 2013. https://doi.org/10.1242/dev.085621.","ista":"Liang H, Xiao G, Yin H, Hippenmeyer S, Horowitz J, Ghashghaei T. 2013. Neural development is dependent on the function of specificity protein 2 in cell cycle progression. Development. 140(3), 552–561."},"quality_controlled":"1","publisher":"Company of Biologists","oa":1,"doi":"10.1242/dev.085621","date_published":"2013-02-01T00:00:00Z","date_created":"2018-12-11T11:56:39Z","page":"552 - 561","day":"01","publication":"Development","year":"2013"},{"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T06:56:39Z","citation":{"chicago":"Hippenmeyer, Simon. “Dissection of Gene Function at Clonal Level Using Mosaic Analysis with Double Markers.” Frontiers in Biology. Springer, 2013. https://doi.org/10.1007/s11515-013-1279-6.","ista":"Hippenmeyer S. 2013. Dissection of gene function at clonal level using mosaic analysis with double markers. Frontiers in Biology. 8(6), 557–568.","mla":"Hippenmeyer, Simon. “Dissection of Gene Function at Clonal Level Using Mosaic Analysis with Double Markers.” Frontiers in Biology, vol. 8, no. 6, Springer, 2013, pp. 557–68, doi:10.1007/s11515-013-1279-6.","ama":"Hippenmeyer S. Dissection of gene function at clonal level using mosaic analysis with double markers. Frontiers in Biology. 2013;8(6):557-568. doi:10.1007/s11515-013-1279-6","apa":"Hippenmeyer, S. (2013). Dissection of gene function at clonal level using mosaic analysis with double markers. Frontiers in Biology. Springer. https://doi.org/10.1007/s11515-013-1279-6","short":"S. Hippenmeyer, Frontiers in Biology 8 (2013) 557–568.","ieee":"S. Hippenmeyer, “Dissection of gene function at clonal level using mosaic analysis with double markers,” Frontiers in Biology, vol. 8, no. 6. Springer, pp. 557–568, 2013."},"title":"Dissection of gene function at clonal level using mosaic analysis with double markers","department":[{"_id":"SiHi"}],"author":[{"orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"publist_id":"4624","_id":"2303","status":"public","article_type":"review","type":"journal_article","day":"03","publication":"Frontiers in Biology","language":[{"iso":"eng"}],"publication_status":"published","year":"2013","date_published":"2013-09-03T00:00:00Z","volume":8,"issue":"6","doi":"10.1007/s11515-013-1279-6","date_created":"2018-12-11T11:56:52Z","page":"557 - 568","oa_version":"None","acknowledgement":"This work was supported by IST Austria institutional funds.","abstract":[{"text":"MADM (Mosaic Analysis with Double Markers) technology offers a genetic approach in mice to visualize and concomitantly manipulate genetically defined cells at clonal level and single cell resolution. MADM employs Cre recombinase/loxP-dependent interchromosomal mitotic recombination to reconstitute two split marker genes—green GFP and red tdTomato—and can label sparse clones of homozygous mutant cells in one color and wild-type cells in the other color in an otherwise unlabeled background. At present, major MADM applications include lineage tracing, single cell labeling, conditional knockouts in small populations of cells and induction of uniparental chromosome disomy to assess effects of genomic imprinting. MADM can be applied universally in the mouse with the sole limitation being the specificity of the promoter controlling Cre recombinase expression. Here I review recent developments and extensions of the MADM technique and give an overview of the major discoveries and progresses enabled by the implementation of the novel genetic MADM tools.","lang":"eng"}],"month":"09","intvolume":" 8","scopus_import":1,"publisher":"Springer","quality_controlled":"1"},{"date_updated":"2021-01-12T07:00:07Z","ddc":["570"],"file_date_updated":"2020-07-14T12:45:50Z","department":[{"_id":"SiHi"}],"_id":"2838","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","pubrep_id":"407","publication_status":"published","file":[{"access_level":"open_access","relation":"main_file","content_type":"application/pdf","file_id":"5160","checksum":"512733b21419574a45f10cabef3d7f81","creator":"system","date_updated":"2020-07-14T12:45:50Z","file_size":4795977,"date_created":"2018-12-12T10:15:38Z","file_name":"IST-2016-407-v1+1_journal.pone.0054285.pdf"}],"language":[{"iso":"eng"}],"volume":8,"issue":"1","abstract":[{"text":"Individuals with Down syndrome (DS) present important motor deficits that derive from altered motor development of infants and young children. DYRK1A, a candidate gene for DS abnormalities has been implicated in motor function due to its expression in motor nuclei in the adult brain, and its overexpression in DS mouse models leads to hyperactivity and altered motor learning. However, its precise role in the adult motor system, or its possible involvement in postnatal locomotor development has not yet been clarified. During the postnatal period we observed time-specific expression of Dyrk1A in discrete subsets of brainstem nuclei and spinal cord motor neurons. Interestingly, we describe for the first time the presence of Dyrk1A in the presynaptic terminal of the neuromuscular junctions and its axonal transport from the facial nucleus, suggesting a function for Dyrk1A in these structures. Relevant to DS, Dyrk1A overexpression in transgenic mice (TgDyrk1A) produces motor developmental alterations possibly contributing to DS motor phenotypes and modifies the numbers of motor cholinergic neurons, suggesting that the kinase may have a role in the development of the brainstem and spinal cord motor system.","lang":"eng"}],"oa_version":"Published Version","scopus_import":1,"month":"01","intvolume":" 8","citation":{"mla":"Arquè Fuste, Gloria, et al. “Dyrk1A Is Dynamically Expressed on Subsets of Motor Neurons and in the Neuromuscular Junction: Possible Role in Down Syndrome.” PLoS One, vol. 8, no. 1, e54285, Public Library of Science, 2013, doi:10.1371/journal.pone.0054285.","short":"G. Arquè Fuste, A. Casanovas, M. Dierssen, PLoS One 8 (2013).","ieee":"G. Arquè Fuste, A. Casanovas, and M. Dierssen, “Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular junction: Possible role in Down syndrome,” PLoS One, vol. 8, no. 1. Public Library of Science, 2013.","apa":"Arquè Fuste, G., Casanovas, A., & Dierssen, M. (2013). Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular junction: Possible role in Down syndrome. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0054285","ama":"Arquè Fuste G, Casanovas A, Dierssen M. Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular junction: Possible role in Down syndrome. PLoS One. 2013;8(1). doi:10.1371/journal.pone.0054285","chicago":"Arquè Fuste, Gloria, Anna Casanovas, and Mara Dierssen. “Dyrk1A Is Dynamically Expressed on Subsets of Motor Neurons and in the Neuromuscular Junction: Possible Role in Down Syndrome.” PLoS One. Public Library of Science, 2013. https://doi.org/10.1371/journal.pone.0054285.","ista":"Arquè Fuste G, Casanovas A, Dierssen M. 2013. Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular junction: Possible role in Down syndrome. PLoS One. 8(1), e54285."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publist_id":"3960","author":[{"id":"3CF33908-F248-11E8-B48F-1D18A9856A87","first_name":"Gloria","full_name":"Arquè Fuste, Gloria","last_name":"Arquè Fuste"},{"last_name":"Casanovas","full_name":"Casanovas, Anna","first_name":"Anna"},{"full_name":"Dierssen, Mara","last_name":"Dierssen","first_name":"Mara"}],"title":"Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular junction: Possible role in Down syndrome","article_number":"e54285","has_accepted_license":"1","year":"2013","day":"16","publication":"PLoS One","doi":"10.1371/journal.pone.0054285","date_published":"2013-01-16T00:00:00Z","date_created":"2018-12-11T11:59:52Z","publisher":"Public Library of Science","quality_controlled":"1","oa":1},{"_id":"2855","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"type":"journal_article","pubrep_id":"405","status":"public","date_updated":"2021-01-12T07:00:16Z","ddc":["570"],"file_date_updated":"2020-07-14T12:45:51Z","department":[{"_id":"SiHi"}],"abstract":[{"text":"Genomic imprinting leads to preferred expression of either the maternal or paternal alleles of a subset of genes. Imprinting is essential for mammalian development, and its deregulation causes many diseases. However, the functional relevance of imprinting at the cellular level is poorly understood for most imprinted genes. We used mosaic analysis with double markers (MADM) in mice to create uniparental disomies (UPDs) and to visualize imprinting effects with single-cell resolution. Although chromosome 12 UPD did not produce detectable phenotypes, chromosome 7 UPD caused highly significant paternal growth dominance in the liver and lung, but not in the brain or heart. A single gene on chromosome 7, encoding the secreted insulin-like growth factor 2 (IGF2), accounts for most of the paternal dominance effect. Mosaic analyses implied additional imprinted loci on chromosome 7 acting cell autonomously to transmit the IGF2 signal. Our study reveals chromosome- and cell-type specificity of genomic imprinting effects.","lang":"eng"}],"oa_version":"Published Version","scopus_import":1,"intvolume":" 3","month":"03","publication_status":"published","language":[{"iso":"eng"}],"file":[{"file_size":1907211,"date_updated":"2020-07-14T12:45:51Z","creator":"system","file_name":"IST-2016-405-v1+1_1-s2.0-S2211124713000612-main.pdf","date_created":"2018-12-12T10:17:20Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_id":"5274","checksum":"6e977b918e81384cd571ec5a9d812289"}],"volume":3,"issue":"3","citation":{"ista":"Hippenmeyer S, Johnson R, Luo L. 2013. Mosaic analysis with double markers reveals cell type specific paternal growth dominance. Cell Reports. 3(3), 960–967.","chicago":"Hippenmeyer, Simon, Randy Johnson, and Liqun Luo. “Mosaic Analysis with Double Markers Reveals Cell Type Specific Paternal Growth Dominance.” Cell Reports. Cell Press, 2013. https://doi.org/10.1016/j.celrep.2013.02.002.","ama":"Hippenmeyer S, Johnson R, Luo L. Mosaic analysis with double markers reveals cell type specific paternal growth dominance. Cell Reports. 2013;3(3):960-967. doi:10.1016/j.celrep.2013.02.002","apa":"Hippenmeyer, S., Johnson, R., & Luo, L. (2013). Mosaic analysis with double markers reveals cell type specific paternal growth dominance. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2013.02.002","short":"S. Hippenmeyer, R. Johnson, L. Luo, Cell Reports 3 (2013) 960–967.","ieee":"S. Hippenmeyer, R. Johnson, and L. Luo, “Mosaic analysis with double markers reveals cell type specific paternal growth dominance,” Cell Reports, vol. 3, no. 3. Cell Press, pp. 960–967, 2013.","mla":"Hippenmeyer, Simon, et al. “Mosaic Analysis with Double Markers Reveals Cell Type Specific Paternal Growth Dominance.” Cell Reports, vol. 3, no. 3, Cell Press, 2013, pp. 960–67, doi:10.1016/j.celrep.2013.02.002."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Johnson, Randy","last_name":"Johnson","first_name":"Randy"},{"full_name":"Luo, Liqun","last_name":"Luo","first_name":"Liqun"}],"publist_id":"3937","title":"Mosaic analysis with double markers reveals cell type specific paternal growth dominance","oa":1,"publisher":"Cell Press","quality_controlled":"1","year":"2013","has_accepted_license":"1","publication":"Cell Reports","day":"28","page":"960 - 967","date_created":"2018-12-11T11:59:57Z","date_published":"2013-03-28T00:00:00Z","doi":"10.1016/j.celrep.2013.02.002"},{"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Liang, Huixuan, Simon Hippenmeyer, and H. Ghashghaei. “A Nestin-Cre Transgenic Mouse Is Insufficient for Recombination in Early Embryonic Neural Progenitors.” Biology Open. The Company of Biologists, 2012. https://doi.org/10.1242/bio.20122287.","ista":"Liang H, Hippenmeyer S, Ghashghaei H. 2012. A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic neural progenitors. Biology open. 1(12), 1200–1203.","mla":"Liang, Huixuan, et al. “A Nestin-Cre Transgenic Mouse Is Insufficient for Recombination in Early Embryonic Neural Progenitors.” Biology Open, vol. 1, no. 12, The Company of Biologists, 2012, pp. 1200–03, doi:10.1242/bio.20122287.","apa":"Liang, H., Hippenmeyer, S., & Ghashghaei, H. (2012). A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic neural progenitors. Biology Open. The Company of Biologists. https://doi.org/10.1242/bio.20122287","ama":"Liang H, Hippenmeyer S, Ghashghaei H. A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic neural progenitors. Biology open. 2012;1(12):1200-1203. doi:10.1242/bio.20122287","short":"H. Liang, S. Hippenmeyer, H. Ghashghaei, Biology Open 1 (2012) 1200–1203.","ieee":"H. Liang, S. Hippenmeyer, and H. Ghashghaei, “A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic neural progenitors,” Biology open, vol. 1, no. 12. The Company of Biologists, pp. 1200–1203, 2012."},"title":"A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic neural progenitors","publist_id":"4682","author":[{"first_name":"Huixuan","full_name":"Liang, Huixuan","last_name":"Liang"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"},{"full_name":"Ghashghaei, H.","last_name":"Ghashghaei","first_name":"H."}],"oa":1,"publisher":"The Company of Biologists","quality_controlled":"1","publication":"Biology open","day":"15","year":"2012","has_accepted_license":"1","date_created":"2018-12-11T11:56:38Z","doi":"10.1242/bio.20122287","date_published":"2012-12-15T00:00:00Z","page":"1200 - 1203","_id":"2263","pubrep_id":"387","status":"public","tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","image":"/images/cc_by_nc_sa.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","short":"CC BY-NC-SA (4.0)"},"type":"journal_article","ddc":["576"],"date_updated":"2021-01-12T06:56:23Z","file_date_updated":"2020-07-14T12:45:35Z","department":[{"_id":"SiHi"}],"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Nestin-cre transgenic mice have been widely used to direct recombination to neural stem cells (NSCs) and intermediate neural progenitor cells (NPCs). Here we report that a readily utilized, and the only commercially available, Nestin-cre line is insufficient for directing recombination in early embryonic NSCs and NPCs. Analysis of recombination efficiency in multiple cre-dependent reporters and a genetic mosaic line revealed consistent temporal and spatial patterns of recombination in NSCs and NPCs. For comparison we utilized a knock-in Emx1cre line and found robust recombination in NSCs and NPCs in ventricular and subventricular zones of the cerebral cortices as early as embryonic day 12.5. In addition we found that the rate of Nestin-cre driven recombination only reaches sufficiently high levels in NSCs and NPCs during late embryonic and early postnatal periods. These findings are important when commercially available cre lines are considered for directing recombination to embryonic NSCs and NPCs."}],"intvolume":" 1","month":"12","scopus_import":1,"language":[{"iso":"eng"}],"file":[{"checksum":"605a1800b81227848c361fd6ba7d22ba","file_id":"4990","content_type":"application/pdf","access_level":"open_access","relation":"main_file","date_created":"2018-12-12T10:13:09Z","file_name":"IST-2015-387-v1+1_1200.full.pdf","date_updated":"2020-07-14T12:45:35Z","file_size":726695,"creator":"system"}],"publication_status":"published","license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","volume":1,"issue":"12"}]