[{"publication_status":"published","language":[{"iso":"eng"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","ec_funded":1,"doi":"10.3389/fcell.2020.574382","publisher":"Frontiers","type":"journal_article","isi":1,"issue":"9","year":"2020","department":[{"_id":"SiHi"}],"has_accepted_license":"1","article_processing_charge":"Yes (via OA deal)","tmp":{"short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png"},"publication":"Frontiers in Cell and Developmental Biology","citation":{"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.","short":"A.H. Hansen, S. Hippenmeyer, Frontiers in Cell and Developmental Biology 8 (2020).","chicago":"Hansen, Andi H, and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms in Radial Projection Neuron Migration in the Developing Cerebral Cortex.” <i>Frontiers in Cell and Developmental Biology</i>. Frontiers, 2020. <a href=\"https://doi.org/10.3389/fcell.2020.574382\">https://doi.org/10.3389/fcell.2020.574382</a>.","apa":"Hansen, A. H., &#38; Hippenmeyer, S. (2020). Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex. <i>Frontiers in Cell and Developmental Biology</i>. Frontiers. <a href=\"https://doi.org/10.3389/fcell.2020.574382\">https://doi.org/10.3389/fcell.2020.574382</a>","ama":"Hansen AH, Hippenmeyer S. Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex. <i>Frontiers in Cell and Developmental Biology</i>. 2020;8(9). doi:<a href=\"https://doi.org/10.3389/fcell.2020.574382\">10.3389/fcell.2020.574382</a>","ieee":"A. H. Hansen and S. Hippenmeyer, “Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex,” <i>Frontiers in Cell and Developmental Biology</i>, vol. 8, no. 9. Frontiers, 2020.","mla":"Hansen, Andi H., and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms in Radial Projection Neuron Migration in the Developing Cerebral Cortex.” <i>Frontiers in Cell and Developmental Biology</i>, vol. 8, no. 9, 574382, Frontiers, 2020, doi:<a href=\"https://doi.org/10.3389/fcell.2020.574382\">10.3389/fcell.2020.574382</a>."},"external_id":{"isi":["000577915900001"],"pmid":["33102480"]},"oa_version":"Published Version","day":"25","intvolume":"         8","date_updated":"2026-09-11T22:31:06Z","quality_controlled":"1","corr_author":"1","date_published":"2020-09-25T00:00:00Z","scopus_import":"1","_id":"8569","month":"09","project":[{"_id":"2625A13E-B435-11E9-9278-68D0E5697425","grant_number":"24812","name":"Molecular mechanisms of radial neuronal migration"},{"_id":"25D61E48-B435-11E9-9278-68D0E5697425","grant_number":"618444","call_identifier":"FP7","name":"Molecular Mechanisms of Cerebral Cortex Development"}],"title":"Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex","status":"public","volume":8,"file_date_updated":"2020-09-28T13:11:17Z","oa":1,"author":[{"first_name":"Andi H","full_name":"Hansen, Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87","last_name":"Hansen"},{"orcid":"0000-0003-2279-1061","first_name":"Simon","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"pmid":1,"ddc":["570"],"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"}],"publication_identifier":{"issn":["2296-634X"]},"article_number":"574382","article_type":"original","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.","fulldoi":"https://doi.org/10.3389/fcell.2020.574382","related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"9962"}]},"file":[{"creator":"dernst","content_type":"application/pdf","file_id":"8584","access_level":"open_access","date_created":"2020-09-28T13:11:17Z","relation":"main_file","file_name":"2020_Frontiers_Hansen.pdf","date_updated":"2020-09-28T13:11:17Z","checksum":"01f731824194c94c81a5da360d997073","file_size":5527139,"success":1}],"date_created":"2020-09-26T06:11:07Z","license":"https://creativecommons.org/licenses/by/4.0/"},{"project":[{"name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain","_id":"25D92700-B435-11E9-9278-68D0E5697425","grant_number":"LS13-002"},{"name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level","_id":"25D7962E-B435-11E9-9278-68D0E5697425","grant_number":"RGP0053/2014"},{"name":"Molecular Mechanisms of Cerebral Cortex Development","_id":"25D61E48-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"618444"},{"call_identifier":"H2020","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"}],"month":"04","volume":149,"status":"public","title":"Epigenetic cues modulating the generation of cell type diversity in the cerebral cortex","oa":1,"file_date_updated":"2020-07-14T12:45:45Z","page":"12-26","corr_author":"1","quality_controlled":"1","date_updated":"2025-04-14T07:43:05Z","scopus_import":"1","date_published":"2019-04-01T00:00:00Z","_id":"27","article_type":"review","abstract":[{"lang":"eng","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."}],"fulldoi":"https://doi.org/10.1111/jnc.14601","file":[{"date_updated":"2020-07-14T12:45:45Z","file_size":889709,"checksum":"db027721a95d36f5de36aadcd0bdf7e6","creator":"kschuh","content_type":"application/pdf","access_level":"open_access","file_id":"7239","date_created":"2020-01-07T13:35:52Z","relation":"main_file","file_name":"2019_Wiley_Amberg.pdf"}],"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","date_created":"2018-12-11T11:44:14Z","author":[{"first_name":"Nicole","orcid":"0000-0002-3183-8207","last_name":"Amberg","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","full_name":"Amberg, Nicole"},{"last_name":"Laukoter","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","full_name":"Laukoter, Susanne","first_name":"Susanne","orcid":"0000-0002-7903-3010"},{"last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","first_name":"Simon","orcid":"0000-0003-2279-1061"}],"ddc":["570"],"has_accepted_license":"1","publication":"Journal of Neurochemistry","tmp":{"short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png"},"article_processing_charge":"Yes (via OA deal)","citation":{"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.","ieee":"N. Amberg, S. Laukoter, and S. Hippenmeyer, “Epigenetic cues modulating the generation of cell type diversity in the cerebral cortex,” <i>Journal of Neurochemistry</i>, vol. 149, no. 1. Wiley, pp. 12–26, 2019.","ama":"Amberg N, Laukoter S, Hippenmeyer S. Epigenetic cues modulating the generation of cell type diversity in the cerebral cortex. <i>Journal of Neurochemistry</i>. 2019;149(1):12-26. doi:<a href=\"https://doi.org/10.1111/jnc.14601\">10.1111/jnc.14601</a>","chicago":"Amberg, Nicole, Susanne Laukoter, and Simon Hippenmeyer. “Epigenetic Cues Modulating the Generation of Cell Type Diversity in the Cerebral Cortex.” <i>Journal of Neurochemistry</i>. Wiley, 2019. <a href=\"https://doi.org/10.1111/jnc.14601\">https://doi.org/10.1111/jnc.14601</a>.","apa":"Amberg, N., Laukoter, S., &#38; Hippenmeyer, S. (2019). Epigenetic cues modulating the generation of cell type diversity in the cerebral cortex. <i>Journal of Neurochemistry</i>. Wiley. <a href=\"https://doi.org/10.1111/jnc.14601\">https://doi.org/10.1111/jnc.14601</a>","short":"N. Amberg, S. Laukoter, S. Hippenmeyer, Journal of Neurochemistry 149 (2019) 12–26.","mla":"Amberg, Nicole, et al. “Epigenetic Cues Modulating the Generation of Cell Type Diversity in the Cerebral Cortex.” <i>Journal of Neurochemistry</i>, vol. 149, no. 1, Wiley, 2019, pp. 12–26, doi:<a href=\"https://doi.org/10.1111/jnc.14601\">10.1111/jnc.14601</a>."},"language":[{"iso":"eng"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publication_status":"published","publisher":"Wiley","ec_funded":1,"doi":"10.1111/jnc.14601","isi":1,"type":"journal_article","year":"2019","issue":"1","department":[{"_id":"SiHi"}],"day":"01","oa_version":"Published Version","intvolume":"       149","external_id":{"isi":["000462680200002"]}},{"intvolume":"         8","day":"21","oa_version":"Published Version","external_id":{"pmid":["30789343"],"isi":["000459380600001"]},"citation":{"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.","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. <i>eLife</i>. 2019;8. doi:<a href=\"https://doi.org/10.7554/eLife.41563\">10.7554/eLife.41563</a>","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,” <i>eLife</i>, vol. 8. eLife Sciences Publications, 2019.","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.” <i>ELife</i>. eLife Sciences Publications, 2019. <a href=\"https://doi.org/10.7554/eLife.41563\">https://doi.org/10.7554/eLife.41563</a>.","apa":"Henderson, N. T., Le Marchand, S. J., Hruska, M., Hippenmeyer, S., Luo, L., &#38; Dalva, M. B. (2019). Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.41563\">https://doi.org/10.7554/eLife.41563</a>","short":"N.T. Henderson, S.J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, M.B. Dalva, ELife 8 (2019).","mla":"Henderson, Nathan T., et al. “Ephrin-B3 Controls Excitatory Synapse Density through Cell-Cell Competition for EphBs.” <i>ELife</i>, vol. 8, e41563, eLife Sciences Publications, 2019, doi:<a href=\"https://doi.org/10.7554/eLife.41563\">10.7554/eLife.41563</a>."},"publication":"eLife","tmp":{"short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png"},"article_processing_charge":"No","has_accepted_license":"1","year":"2019","department":[{"_id":"SiHi"}],"isi":1,"type":"journal_article","publisher":"eLife Sciences Publications","doi":"10.7554/eLife.41563","language":[{"iso":"eng"}],"publication_status":"published","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","date_created":"2019-03-10T22:59:20Z","file":[{"date_updated":"2020-07-14T12:47:19Z","checksum":"7b0800d003f14cd06b1802dea0c52941","file_size":7260753,"access_level":"open_access","file_id":"6098","content_type":"application/pdf","creator":"dernst","file_name":"2019_eLife_Henderson.pdf","relation":"main_file","date_created":"2019-03-11T16:15:37Z"}],"fulldoi":"https://doi.org/10.7554/eLife.41563","article_number":"e41563","abstract":[{"lang":"eng","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."}],"ddc":["570"],"pmid":1,"author":[{"full_name":"Henderson, Nathan T.","last_name":"Henderson","first_name":"Nathan T."},{"first_name":"Sylvain J.","last_name":"Le Marchand","full_name":"Le Marchand, Sylvain J."},{"first_name":"Martin","last_name":"Hruska","full_name":"Hruska, Martin"},{"first_name":"Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon"},{"first_name":"Liqun","full_name":"Luo, Liqun","last_name":"Luo"},{"last_name":"Dalva","full_name":"Dalva, Matthew B.","first_name":"Matthew B."}],"oa":1,"file_date_updated":"2020-07-14T12:47:19Z","volume":8,"status":"public","title":"Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs","month":"02","_id":"6091","scopus_import":"1","date_published":"2019-02-21T00:00:00Z","quality_controlled":"1","date_updated":"2023-08-24T14:50:50Z"},{"author":[{"last_name":"Amberg","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","full_name":"Amberg, Nicole","first_name":"Nicole","orcid":"0000-0002-3183-8207"},{"last_name":"Sotiropoulou","full_name":"Sotiropoulou, Panagiota A.","first_name":"Panagiota A."},{"first_name":"Gerwin","last_name":"Heller","full_name":"Heller, Gerwin"},{"last_name":"Lichtenberger","full_name":"Lichtenberger, Beate M.","first_name":"Beate M."},{"last_name":"Holcmann","full_name":"Holcmann, Martin","first_name":"Martin"},{"first_name":"Bahar","last_name":"Camurdanoglu","full_name":"Camurdanoglu, Bahar"},{"first_name":"Temenuschka","last_name":"Baykuscheva-Gentscheva","full_name":"Baykuscheva-Gentscheva, Temenuschka"},{"last_name":"Blanpain","full_name":"Blanpain, Cedric","first_name":"Cedric"},{"last_name":"Sibilia","full_name":"Sibilia, Maria","first_name":"Maria"}],"ddc":["570"],"fulldoi":"https://doi.org/10.1016/j.isci.2019.04.018","file":[{"file_size":8365970,"checksum":"a9ad2296726c9474ad5860c9c2f53622","date_updated":"2020-07-14T12:47:30Z","file_name":"2019_iScience_Amberg.pdf","relation":"main_file","date_created":"2019-05-14T11:51:51Z","file_id":"6452","access_level":"open_access","content_type":"application/pdf","creator":"dernst"}],"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"}],"publication_identifier":{"issn":["2589-0042"]},"date_created":"2019-05-14T11:47:40Z","date_updated":"2023-09-08T11:38:04Z","quality_controlled":"1","_id":"6451","date_published":"2019-05-31T00:00:00Z","month":"05","page":"243-256","file_date_updated":"2020-07-14T12:47:30Z","oa":1,"title":"EGFR controls hair shaft differentiation in a p53-independent manner","volume":15,"status":"public","external_id":{"isi":["000470104600022"]},"day":"31","oa_version":"Published Version","intvolume":"        15","doi":"10.1016/j.isci.2019.04.018","publisher":"Elsevier","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publication_status":"published","language":[{"iso":"eng"}],"year":"2019","department":[{"_id":"SiHi"}],"type":"journal_article","isi":1,"article_processing_charge":"No","tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","image":"/images/cc_by_nc_nd.png","short":"CC BY-NC-ND (4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"publication":"iScience","has_accepted_license":"1","citation":{"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. <i>IScience</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.isci.2019.04.018\">https://doi.org/10.1016/j.isci.2019.04.018</a>","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.” <i>IScience</i>. Elsevier, 2019. <a href=\"https://doi.org/10.1016/j.isci.2019.04.018\">https://doi.org/10.1016/j.isci.2019.04.018</a>.","ieee":"N. Amberg <i>et al.</i>, “EGFR controls hair shaft differentiation in a p53-independent manner,” <i>iScience</i>, vol. 15. Elsevier, pp. 243–256, 2019.","ama":"Amberg N, Sotiropoulou PA, Heller G, et al. EGFR controls hair shaft differentiation in a p53-independent manner. <i>iScience</i>. 2019;15:243-256. doi:<a href=\"https://doi.org/10.1016/j.isci.2019.04.018\">10.1016/j.isci.2019.04.018</a>","mla":"Amberg, Nicole, et al. “EGFR Controls Hair Shaft Differentiation in a P53-Independent Manner.” <i>IScience</i>, vol. 15, Elsevier, 2019, pp. 243–56, doi:<a href=\"https://doi.org/10.1016/j.isci.2019.04.018\">10.1016/j.isci.2019.04.018</a>.","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."}},{"date_published":"2019-04-03T00:00:00Z","scopus_import":"1","_id":"6454","date_updated":"2025-04-14T07:43:05Z","quality_controlled":"1","title":"Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members","volume":102,"status":"public","page":"159-172.e7","file_date_updated":"2020-07-14T12:47:30Z","oa":1,"month":"04","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"}],"pmid":1,"ddc":["570"],"author":[{"first_name":"G","last_name":"Ortiz-Álvarez","full_name":"Ortiz-Álvarez, G"},{"last_name":"Daclin","full_name":"Daclin, M","first_name":"M"},{"last_name":"Shihavuddin","full_name":"Shihavuddin, A","first_name":"A"},{"full_name":"Lansade, P","last_name":"Lansade","first_name":"P"},{"first_name":"A","full_name":"Fortoul, A","last_name":"Fortoul"},{"first_name":"M","last_name":"Faucourt","full_name":"Faucourt, M"},{"last_name":"Clavreul","full_name":"Clavreul, S","first_name":"S"},{"last_name":"Lalioti","full_name":"Lalioti, ME","first_name":"ME"},{"last_name":"Taraviras","full_name":"Taraviras, S","first_name":"S"},{"last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","first_name":"Simon","orcid":"0000-0003-2279-1061"},{"first_name":"J","last_name":"Livet","full_name":"Livet, J"},{"first_name":"A","last_name":"Meunier","full_name":"Meunier, A"},{"first_name":"A","last_name":"Genovesio","full_name":"Genovesio, A"},{"first_name":"N","full_name":"Spassky, N","last_name":"Spassky"}],"date_created":"2019-05-14T13:06:30Z","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"}],"publication_identifier":{"eissn":["1097-4199"],"issn":["0896-6273"]},"file":[{"date_updated":"2020-07-14T12:47:30Z","file_size":7288572,"checksum":"1fb6e195c583eb0c5cabf26f69ff6675","file_id":"6457","access_level":"open_access","content_type":"application/pdf","creator":"dernst","file_name":"2019_Neuron_Ortiz.pdf","relation":"main_file","date_created":"2019-05-15T09:28:41Z"}],"fulldoi":"https://doi.org/10.1016/j.neuron.2019.01.051","type":"journal_article","isi":1,"department":[{"_id":"SiHi"}],"issue":"1","year":"2019","language":[{"iso":"eng"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publication_status":"published","ec_funded":1,"doi":"10.1016/j.neuron.2019.01.051","publisher":"Elsevier","citation":{"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.","mla":"Ortiz-Álvarez, G., et al. “Adult Neural Stem Cells and Multiciliated Ependymal Cells Share a Common Lineage Regulated by the Geminin Family Members.” <i>Neuron</i>, vol. 102, no. 1, Elsevier, 2019, p. 159–172.e7, doi:<a href=\"https://doi.org/10.1016/j.neuron.2019.01.051\">10.1016/j.neuron.2019.01.051</a>.","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. <i>Neuron</i>. 2019;102(1):159-172.e7. doi:<a href=\"https://doi.org/10.1016/j.neuron.2019.01.051\">10.1016/j.neuron.2019.01.051</a>","ieee":"G. Ortiz-Álvarez <i>et al.</i>, “Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members,” <i>Neuron</i>, vol. 102, no. 1. Elsevier, p. 159–172.e7, 2019.","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. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2019.01.051\">https://doi.org/10.1016/j.neuron.2019.01.051</a>","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.","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.” <i>Neuron</i>. Elsevier, 2019. <a href=\"https://doi.org/10.1016/j.neuron.2019.01.051\">https://doi.org/10.1016/j.neuron.2019.01.051</a>."},"has_accepted_license":"1","tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","image":"/images/cc_by_nc_nd.png","short":"CC BY-NC-ND (4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"article_processing_charge":"No","publication":"Neuron","external_id":{"pmid":["30824354"],"isi":["000463337900018"]},"intvolume":"       102","day":"03","oa_version":"Published Version"},{"month":"05","project":[{"grant_number":"725780","call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"},{"name":"Role of Eed in neural stem cell lineage progression","_id":"268F8446-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"T01031"}],"title":"Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex","status":"public","volume":364,"oa":1,"date_updated":"2026-06-18T19:04:26Z","quality_controlled":"1","date_published":"2019-05-10T00:00:00Z","scopus_import":"1","_id":"6455","abstract":[{"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.","lang":"eng"}],"publication_identifier":{"issn":["0036-8075"],"eissn":["1095-9203"]},"article_number":"eaav2522","article_type":"original","fulldoi":"https://doi.org/10.1126/science.aav2522","related_material":{"link":[{"url":"https://ist.ac.at/en/news/how-to-generate-a-brain-of-correct-size-and-composition/","description":"News on IST Homepage","relation":"press_release"}]},"date_created":"2019-05-14T13:07:47Z","author":[{"first_name":"L","last_name":"Telley","full_name":"Telley, L"},{"full_name":"Agirman, G","last_name":"Agirman","first_name":"G"},{"full_name":"Prados, J","last_name":"Prados","first_name":"J"},{"full_name":"Amberg, Nicole","last_name":"Amberg","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-3183-8207","first_name":"Nicole"},{"first_name":"S","full_name":"Fièvre, S","last_name":"Fièvre"},{"full_name":"Oberst, P","last_name":"Oberst","first_name":"P"},{"full_name":"Bartolini, G","last_name":"Bartolini","first_name":"G"},{"first_name":"I","full_name":"Vitali, I","last_name":"Vitali"},{"last_name":"Cadilhac","full_name":"Cadilhac, C","first_name":"C"},{"full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","first_name":"Simon"},{"full_name":"Nguyen, L","last_name":"Nguyen","first_name":"L"},{"first_name":"A","last_name":"Dayer","full_name":"Dayer, A"},{"first_name":"D","full_name":"Jabaudon, D","last_name":"Jabaudon"}],"pmid":1,"ddc":["570"],"main_file_link":[{"url":"https://orbi.uliege.be/bitstream/2268/239604/1/Telley_Agirman_Science2019.pdf","open_access":"1"}],"article_processing_charge":"No","publication":"Science","citation":{"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.","mla":"Telley, L., et al. “Temporal Patterning of Apical Progenitors and Their Daughter Neurons in the Developing Neocortex.” <i>Science</i>, vol. 364, no. 6440, eaav2522, AAAS, 2019, doi:<a href=\"https://doi.org/10.1126/science.aav2522\">10.1126/science.aav2522</a>.","ieee":"L. Telley <i>et al.</i>, “Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex,” <i>Science</i>, vol. 364, no. 6440. AAAS, 2019.","ama":"Telley L, Agirman G, Prados J, et al. Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex. <i>Science</i>. 2019;364(6440). doi:<a href=\"https://doi.org/10.1126/science.aav2522\">10.1126/science.aav2522</a>","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.” <i>Science</i>. AAAS, 2019. <a href=\"https://doi.org/10.1126/science.aav2522\">https://doi.org/10.1126/science.aav2522</a>.","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. <i>Science</i>. AAAS. <a href=\"https://doi.org/10.1126/science.aav2522\">https://doi.org/10.1126/science.aav2522</a>","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)."},"publication_status":"published","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","language":[{"iso":"eng"}],"ec_funded":1,"doi":"10.1126/science.aav2522","publisher":"AAAS","type":"journal_article","isi":1,"department":[{"_id":"SiHi"}],"year":"2019","issue":"6440","oa_version":"Published Version","day":"10","intvolume":"       364","external_id":{"isi":["000467631800034"],"pmid":["31073041"]}},{"quality_controlled":"1","date_updated":"2025-04-14T07:43:05Z","scopus_import":"1","date_published":"2019-09-01T00:00:00Z","_id":"6844","project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","call_identifier":"H2020","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425"}],"month":"09","status":"public","volume":235,"title":"A mathematical insight into cell labelling experiments for clonal analysis","oa":1,"page":"686-696","file_date_updated":"2020-07-14T12:47:42Z","author":[{"last_name":"Picco","full_name":"Picco, Noemi","first_name":"Noemi"},{"full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","first_name":"Simon"},{"first_name":"Julio","id":"3C70A038-F248-11E8-B48F-1D18A9856A87","last_name":"Rodarte","full_name":"Rodarte, Julio"},{"last_name":"Streicher","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","full_name":"Streicher, Carmen","first_name":"Carmen"},{"last_name":"Molnár","full_name":"Molnár, Zoltán","first_name":"Zoltán"},{"first_name":"Philip K.","last_name":"Maini","full_name":"Maini, Philip K."},{"first_name":"Thomas E.","full_name":"Woolley, Thomas E.","last_name":"Woolley"}],"ddc":["570"],"article_type":"original","publication_identifier":{"eissn":["1469-7580"],"issn":["0021-8782"]},"abstract":[{"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.","lang":"eng"}],"fulldoi":"https://doi.org/10.1111/joa.13001","file":[{"relation":"main_file","file_name":"2019_JournalAnatomy_Picco.pdf","date_created":"2019-09-02T12:05:18Z","content_type":"application/pdf","creator":"dernst","file_id":"6845","access_level":"open_access","file_size":1192994,"checksum":"160f960844b204057f20896e0e1f8ee7","date_updated":"2020-07-14T12:47:42Z"}],"license":"https://creativecommons.org/licenses/by-nc/4.0/","date_created":"2019-09-02T11:57:28Z","publication_status":"published","language":[{"iso":"eng"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","publisher":"Wiley","doi":"10.1111/joa.13001","ec_funded":1,"isi":1,"type":"journal_article","department":[{"_id":"SiHi"}],"year":"2019","issue":"3","has_accepted_license":"1","publication":"Journal of Anatomy","tmp":{"short":"CC BY-NC (4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc/4.0/legalcode","name":"Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)","image":"/images/cc_by_nc.png"},"article_processing_charge":"No","citation":{"apa":"Picco, N., Hippenmeyer, S., Rodarte, J., Streicher, C., Molnár, Z., Maini, P. K., &#38; Woolley, T. E. (2019). A mathematical insight into cell labelling experiments for clonal analysis. <i>Journal of Anatomy</i>. Wiley. <a href=\"https://doi.org/10.1111/joa.13001\">https://doi.org/10.1111/joa.13001</a>","short":"N. Picco, S. Hippenmeyer, J. Rodarte, C. Streicher, Z. Molnár, P.K. Maini, T.E. Woolley, Journal of Anatomy 235 (2019) 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.” <i>Journal of Anatomy</i>. Wiley, 2019. <a href=\"https://doi.org/10.1111/joa.13001\">https://doi.org/10.1111/joa.13001</a>.","ieee":"N. Picco <i>et al.</i>, “A mathematical insight into cell labelling experiments for clonal analysis,” <i>Journal of Anatomy</i>, vol. 235, no. 3. Wiley, pp. 686–696, 2019.","ama":"Picco N, Hippenmeyer S, Rodarte J, et al. A mathematical insight into cell labelling experiments for clonal analysis. <i>Journal of Anatomy</i>. 2019;235(3):686-696. doi:<a href=\"https://doi.org/10.1111/joa.13001\">10.1111/joa.13001</a>","mla":"Picco, Noemi, et al. “A Mathematical Insight into Cell Labelling Experiments for Clonal Analysis.” <i>Journal of Anatomy</i>, vol. 235, no. 3, Wiley, 2019, pp. 686–96, doi:<a href=\"https://doi.org/10.1111/joa.13001\">10.1111/joa.13001</a>.","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."},"external_id":{"isi":["000482426800017"]},"oa_version":"Published Version","day":"01","intvolume":"       235"},{"pmid":1,"ddc":["570"],"author":[{"full_name":"Cheung, Giselle T","id":"471195F6-F248-11E8-B48F-1D18A9856A87","last_name":"Cheung","orcid":"0000-0001-8457-2572","first_name":"Giselle T"},{"last_name":"Cousin","full_name":"Cousin, Michael A.","first_name":"Michael A."}],"date_created":"2019-11-12T14:37:08Z","abstract":[{"lang":"eng","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."}],"publication_identifier":{"eissn":["1471-4159"],"issn":["0022-3042"]},"article_type":"original","file":[{"date_updated":"2020-07-14T12:47:47Z","checksum":"ec1fb2aebb874009bc309adaada6e1d7","file_size":4334962,"file_id":"7452","access_level":"open_access","creator":"dernst","content_type":"application/pdf","date_created":"2020-02-05T10:30:02Z","file_name":"2019_JournNeurochemistry_Cheung.pdf","relation":"main_file"}],"fulldoi":"https://doi.org/10.1111/jnc.14862","date_published":"2019-12-01T00:00:00Z","scopus_import":"1","_id":"7005","date_updated":"2023-08-30T07:21:50Z","quality_controlled":"1","title":"Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction","status":"public","volume":151,"page":"570-583","file_date_updated":"2020-07-14T12:47:47Z","oa":1,"month":"12","external_id":{"isi":["000490703100001"],"pmid":["31479508"]},"intvolume":"       151","oa_version":"Published Version","day":"01","type":"journal_article","isi":1,"issue":"5","year":"2019","department":[{"_id":"SiHi"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","publication_status":"published","language":[{"iso":"eng"}],"doi":"10.1111/jnc.14862","publisher":"Wiley","citation":{"mla":"Cheung, Giselle T., and Michael A. Cousin. “Synaptic Vesicle Generation from Activity‐dependent Bulk Endosomes Requires a Dephosphorylation‐dependent Dynamin–Syndapin Interaction.” <i>Journal of Neurochemistry</i>, vol. 151, no. 5, Wiley, 2019, pp. 570–83, doi:<a href=\"https://doi.org/10.1111/jnc.14862\">10.1111/jnc.14862</a>.","chicago":"Cheung, Giselle T, and Michael A. Cousin. “Synaptic Vesicle Generation from Activity‐dependent Bulk Endosomes Requires a Dephosphorylation‐dependent Dynamin–Syndapin Interaction.” <i>Journal of Neurochemistry</i>. Wiley, 2019. <a href=\"https://doi.org/10.1111/jnc.14862\">https://doi.org/10.1111/jnc.14862</a>.","short":"G.T. Cheung, M.A. Cousin, Journal of Neurochemistry 151 (2019) 570–583.","apa":"Cheung, G. T., &#38; Cousin, M. A. (2019). Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction. <i>Journal of Neurochemistry</i>. Wiley. <a href=\"https://doi.org/10.1111/jnc.14862\">https://doi.org/10.1111/jnc.14862</a>","ama":"Cheung GT, Cousin MA. Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction. <i>Journal of Neurochemistry</i>. 2019;151(5):570-583. doi:<a href=\"https://doi.org/10.1111/jnc.14862\">10.1111/jnc.14862</a>","ieee":"G. T. Cheung and M. A. Cousin, “Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction,” <i>Journal of Neurochemistry</i>, vol. 151, no. 5. Wiley, pp. 570–583, 2019.","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."},"has_accepted_license":"1","tmp":{"short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png"},"article_processing_charge":"No","publication":"Journal of Neurochemistry"},{"author":[{"full_name":"Llorca, Alfredo","last_name":"Llorca","first_name":"Alfredo"},{"full_name":"Ciceri, Gabriele","last_name":"Ciceri","first_name":"Gabriele"},{"orcid":"0000-0002-8483-8753","first_name":"Robert J","full_name":"Beattie, Robert J","last_name":"Beattie","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Fong Kuan","full_name":"Wong, Fong Kuan","last_name":"Wong"},{"full_name":"Diana, Giovanni","last_name":"Diana","first_name":"Giovanni"},{"last_name":"Serafeimidou-Pouliou","full_name":"Serafeimidou-Pouliou, Eleni","first_name":"Eleni"},{"last_name":"Fernández-Otero","full_name":"Fernández-Otero, Marian","first_name":"Marian"},{"full_name":"Streicher, Carmen","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","last_name":"Streicher","first_name":"Carmen"},{"last_name":"Arnold","full_name":"Arnold, Sebastian J.","first_name":"Sebastian J."},{"first_name":"Martin","last_name":"Meyer","full_name":"Meyer, Martin"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","first_name":"Simon","orcid":"0000-0003-2279-1061"},{"full_name":"Maravall, Miguel","last_name":"Maravall","first_name":"Miguel"},{"full_name":"Marín, Oscar","last_name":"Marín","first_name":"Oscar"}],"ddc":["570"],"pmid":1,"article_type":"original","publication_identifier":{"eissn":["2050-084X"]},"article_number":"e51381","abstract":[{"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.","lang":"eng"}],"file":[{"access_level":"open_access","file_id":"7503","creator":"dernst","content_type":"application/pdf","date_created":"2020-02-18T15:19:26Z","file_name":"2019_eLife_Llorca.pdf","relation":"main_file","date_updated":"2020-07-14T12:47:53Z","checksum":"b460ecc33e1a68265e7adea775021f3a","file_size":2960543}],"fulldoi":"https://doi.org/10.7554/eLife.51381","date_created":"2019-12-22T23:00:42Z","quality_controlled":"1","date_updated":"2026-04-03T09:46:33Z","scopus_import":"1","date_published":"2019-11-18T00:00:00Z","_id":"7202","project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"725780"},{"_id":"264E56E2-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"M02416","name":"Molecular Mechanisms Regulating Gliogenesis in the Neocortex"}],"month":"11","status":"public","volume":8,"title":"A stochastic framework of neurogenesis underlies the assembly of neocortical cytoarchitecture","oa":1,"file_date_updated":"2020-07-14T12:47:53Z","external_id":{"isi":["000508156800001"],"pmid":["31736464"]},"oa_version":"Published Version","day":"18","intvolume":"         8","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","language":[{"iso":"eng"}],"publication_status":"published","publisher":"eLife Sciences Publications","doi":"10.7554/eLife.51381","ec_funded":1,"isi":1,"type":"journal_article","department":[{"_id":"SiHi"}],"year":"2019","has_accepted_license":"1","publication":"eLife","tmp":{"short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png"},"article_processing_charge":"No","citation":{"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. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.51381\">https://doi.org/10.7554/eLife.51381</a>","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.” <i>ELife</i>. eLife Sciences Publications, 2019. <a href=\"https://doi.org/10.7554/eLife.51381\">https://doi.org/10.7554/eLife.51381</a>.","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 <i>et al.</i>, “A stochastic framework of neurogenesis underlies the assembly of neocortical cytoarchitecture,” <i>eLife</i>, vol. 8. eLife Sciences Publications, 2019.","ama":"Llorca A, Ciceri G, Beattie RJ, et al. A stochastic framework of neurogenesis underlies the assembly of neocortical cytoarchitecture. <i>eLife</i>. 2019;8. doi:<a href=\"https://doi.org/10.7554/eLife.51381\">10.7554/eLife.51381</a>","mla":"Llorca, Alfredo, et al. “A Stochastic Framework of Neurogenesis Underlies the Assembly of Neocortical Cytoarchitecture.” <i>ELife</i>, vol. 8, e51381, eLife Sciences Publications, 2019, doi:<a href=\"https://doi.org/10.7554/eLife.51381\">10.7554/eLife.51381</a>.","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."}},{"publication":"PLoS Genetics","article_processing_charge":"No","tmp":{"short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png"},"has_accepted_license":"1","citation":{"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.” <i>PLoS Genetics</i>. Public Library of Science, 2019. <a href=\"https://doi.org/10.1371/journal.pgen.1008268\">https://doi.org/10.1371/journal.pgen.1008268</a>.","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).","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. <i>PLoS Genetics</i>. Public Library of Science. <a href=\"https://doi.org/10.1371/journal.pgen.1008268\">https://doi.org/10.1371/journal.pgen.1008268</a>","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. <i>PLoS Genetics</i>. 2019;15(7). doi:<a href=\"https://doi.org/10.1371/journal.pgen.1008268\">10.1371/journal.pgen.1008268</a>","ieee":"D. Andergassen <i>et al.</i>, “The Airn lncRNA does not require any DNA elements within its locus to silence distant imprinted genes,” <i>PLoS Genetics</i>, vol. 15, no. 7. Public Library of Science, 2019.","mla":"Andergassen, Daniel, et al. “The Airn LncRNA Does Not Require Any DNA Elements within Its Locus to Silence Distant Imprinted Genes.” <i>PLoS Genetics</i>, vol. 15, no. 7, e1008268, Public Library of Science, 2019, doi:<a href=\"https://doi.org/10.1371/journal.pgen.1008268\">10.1371/journal.pgen.1008268</a>.","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."},"publisher":"Public Library of Science","doi":"10.1371/journal.pgen.1008268","language":[{"iso":"eng"}],"publication_status":"published","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","year":"2019","department":[{"_id":"SiHi"}],"issue":"7","isi":1,"type":"journal_article","day":"22","oa_version":"Published Version","intvolume":"        15","external_id":{"pmid":["31329595"],"isi":["000478689100025"]},"month":"07","oa":1,"file_date_updated":"2020-07-14T12:47:57Z","status":"public","volume":15,"title":"The Airn lncRNA does not require any DNA elements within its locus to silence distant imprinted genes","quality_controlled":"1","corr_author":"1","date_updated":"2024-10-09T20:59:14Z","_id":"7399","scopus_import":"1","date_published":"2019-07-22T00:00:00Z","file":[{"file_size":2302307,"checksum":"2f51fc91e4a4199827adc51d432ad864","date_updated":"2020-07-14T12:47:57Z","file_name":"2019_PlosGenetics_Andergassen.pdf","relation":"main_file","date_created":"2020-02-04T10:11:55Z","access_level":"open_access","file_id":"7446","creator":"dernst","content_type":"application/pdf"}],"fulldoi":"https://doi.org/10.1371/journal.pgen.1008268","publication_identifier":{"issn":["1553-7404"]},"article_number":"e1008268","article_type":"original","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"}],"date_created":"2020-01-29T16:14:07Z","author":[{"first_name":"Daniel","last_name":"Andergassen","full_name":"Andergassen, Daniel"},{"first_name":"Markus","last_name":"Muckenhuber","full_name":"Muckenhuber, Markus"},{"first_name":"Philipp C.","full_name":"Bammer, Philipp C.","last_name":"Bammer"},{"last_name":"Kulinski","full_name":"Kulinski, Tomasz M.","first_name":"Tomasz M."},{"first_name":"Hans-Christian","full_name":"Theussl, Hans-Christian","last_name":"Theussl"},{"first_name":"Takahiko","last_name":"Shimizu","full_name":"Shimizu, Takahiko"},{"full_name":"Penninger, Josef M.","last_name":"Penninger","first_name":"Josef M."},{"orcid":"0000-0002-7462-0048","first_name":"Florian","full_name":"Pauler, Florian","last_name":"Pauler","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Hudson","full_name":"Hudson, Quanah J.","first_name":"Quanah J."}],"pmid":1,"ddc":["570"]},{"related_material":{"record":[{"id":"7902","status":"public","relation":"part_of_dissertation"}]},"fulldoi":"https://doi.org/10.1016/j.neuron.2019.08.021","publication_identifier":{"issn":["0896-6273"],"eissn":["1097-4199"]},"article_type":"letter_note","date_created":"2019-08-25T22:00:50Z","author":[{"id":"475990FE-F248-11E8-B48F-1D18A9856A87","last_name":"Contreras","full_name":"Contreras, Ximena","first_name":"Ximena"},{"last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","first_name":"Simon","orcid":"0000-0003-2279-1061"}],"pmid":1,"ddc":["570"],"main_file_link":[{"url":"https://doi.org/10.1016/j.neuron.2019.08.021","open_access":"1"}],"month":"09","page":"750-752","oa":1,"title":"Memo1 tiles the radial glial cell grid","volume":103,"status":"public","date_updated":"2026-09-11T22:30:21Z","quality_controlled":"1","_id":"6830","date_published":"2019-09-04T00:00:00Z","scopus_import":"1","oa_version":"Published Version","day":"04","intvolume":"       103","external_id":{"isi":["000484400200002"],"pmid":["31487522"]},"article_processing_charge":"No","publication":"Neuron","citation":{"ista":"Contreras X, Hippenmeyer S. 2019. Memo1 tiles the radial glial cell grid. Neuron. 103(5), 750–752.","ieee":"X. Contreras and S. Hippenmeyer, “Memo1 tiles the radial glial cell grid,” <i>Neuron</i>, vol. 103, no. 5. Elsevier, pp. 750–752, 2019.","ama":"Contreras X, Hippenmeyer S. Memo1 tiles the radial glial cell grid. <i>Neuron</i>. 2019;103(5):750-752. doi:<a href=\"https://doi.org/10.1016/j.neuron.2019.08.021\">10.1016/j.neuron.2019.08.021</a>","short":"X. Contreras, S. Hippenmeyer, Neuron 103 (2019) 750–752.","chicago":"Contreras, Ximena, and Simon Hippenmeyer. “Memo1 Tiles the Radial Glial Cell Grid.” <i>Neuron</i>. Elsevier, 2019. <a href=\"https://doi.org/10.1016/j.neuron.2019.08.021\">https://doi.org/10.1016/j.neuron.2019.08.021</a>.","apa":"Contreras, X., &#38; Hippenmeyer, S. (2019). Memo1 tiles the radial glial cell grid. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2019.08.021\">https://doi.org/10.1016/j.neuron.2019.08.021</a>","mla":"Contreras, Ximena, and Simon Hippenmeyer. “Memo1 Tiles the Radial Glial Cell Grid.” <i>Neuron</i>, vol. 103, no. 5, Elsevier, 2019, pp. 750–52, doi:<a href=\"https://doi.org/10.1016/j.neuron.2019.08.021\">10.1016/j.neuron.2019.08.021</a>."},"doi":"10.1016/j.neuron.2019.08.021","publisher":"Elsevier","publication_status":"published","language":[{"iso":"eng"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","year":"2019","department":[{"_id":"SiHi"}],"issue":"5","type":"journal_article","isi":1},{"external_id":{"isi":["000450976700002"]},"oa_version":"Published Version","day":"03","intvolume":"        19","publisher":"BioMed Central","doi":"10.1186/s12864-018-5173-0","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","language":[{"iso":"eng"}],"publication_status":"published","year":"2018","department":[{"_id":"SiHi"}],"issue":"1","isi":1,"type":"journal_article","publication":"BMC Genomics","article_processing_charge":"No","tmp":{"short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png"},"has_accepted_license":"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).","mla":"Higareda Almaraz, Juan, et al. “Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes.” <i>BMC Genomics</i>, vol. 19, no. 1, BioMed Central, 2018, doi:<a href=\"https://doi.org/10.1186/s12864-018-5173-0\">10.1186/s12864-018-5173-0</a>.","ieee":"J. Higareda Almaraz <i>et al.</i>, “Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes,” <i>BMC Genomics</i>, vol. 19, no. 1. BioMed Central, 2018.","ama":"Higareda Almaraz J, Karbiener M, Giroud M, et al. Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. <i>BMC Genomics</i>. 2018;19(1). doi:<a href=\"https://doi.org/10.1186/s12864-018-5173-0\">10.1186/s12864-018-5173-0</a>","apa":"Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T., Herzig, S., &#38; Scheideler, M. (2018). Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. <i>BMC Genomics</i>. BioMed Central. <a href=\"https://doi.org/10.1186/s12864-018-5173-0\">https://doi.org/10.1186/s12864-018-5173-0</a>","short":"J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S. Herzig, M. Scheideler, BMC Genomics 19 (2018).","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.” <i>BMC Genomics</i>. BioMed Central, 2018. <a href=\"https://doi.org/10.1186/s12864-018-5173-0\">https://doi.org/10.1186/s12864-018-5173-0</a>."},"author":[{"last_name":"Higareda Almaraz","full_name":"Higareda Almaraz, Juan","first_name":"Juan"},{"first_name":"Michael","last_name":"Karbiener","full_name":"Karbiener, Michael"},{"first_name":"Maude","full_name":"Giroud, Maude","last_name":"Giroud"},{"first_name":"Florian","orcid":"0000-0002-7462-0048","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","last_name":"Pauler","full_name":"Pauler, Florian"},{"first_name":"Teresa","last_name":"Gerhalter","full_name":"Gerhalter, Teresa"},{"last_name":"Herzig","full_name":"Herzig, Stephan","first_name":"Stephan"},{"first_name":"Marcel","full_name":"Scheideler, Marcel","last_name":"Scheideler"}],"ddc":["570"],"fulldoi":"https://doi.org/10.1186/s12864-018-5173-0","file":[{"date_updated":"2020-07-14T12:45:23Z","checksum":"a56516e734dab589dc7f3e1915973b4d","file_size":4629784,"creator":"dernst","content_type":"application/pdf","file_id":"5712","access_level":"open_access","relation":"main_file","file_name":"2018_BMCGenomics_Higareda.pdf","date_created":"2018-12-17T14:52:57Z"}],"related_material":{"record":[{"relation":"research_data","id":"9807","status":"public"},{"status":"public","relation":"research_data","id":"9808"}]},"acknowledgement":"This work was funded by the German Centre for Diabetes Research (DZD) and the Austrian Science Fund (FWF, P25729-B19).","article_type":"original","publication_identifier":{"issn":["1471-2164"]},"abstract":[{"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.","lang":"eng"}],"date_created":"2018-12-11T11:44:12Z","quality_controlled":"1","date_updated":"2023-09-13T09:10:47Z","_id":"20","scopus_import":"1","publist_id":"8035","date_published":"2018-11-03T00:00:00Z","month":"11","oa":1,"file_date_updated":"2020-07-14T12:45:23Z","volume":19,"status":"public","title":"Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes"},{"month":"11","article_processing_charge":"No","citation":{"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, <a href=\"https://doi.org/10.6084/m9.figshare.7295339.v1\">10.6084/m9.figshare.7295339.v1</a>.","ieee":"J. Higareda Almaraz <i>et al.</i>, “Additional file 1: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes.” Springer Nature, 2018.","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:<a href=\"https://doi.org/10.6084/m9.figshare.7295339.v1\">10.6084/m9.figshare.7295339.v1</a>","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. <a href=\"https://doi.org/10.6084/m9.figshare.7295339.v1\">https://doi.org/10.6084/m9.figshare.7295339.v1</a>.","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., &#38; Scheideler, M. (2018). Additional file 1: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. Springer Nature. <a href=\"https://doi.org/10.6084/m9.figshare.7295339.v1\">https://doi.org/10.6084/m9.figshare.7295339.v1</a>","mla":"Higareda Almaraz, Juan, et al. <i>Additional File 1: Of Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes</i>. Springer Nature, 2018, doi:<a href=\"https://doi.org/10.6084/m9.figshare.7295339.v1\">10.6084/m9.figshare.7295339.v1</a>."},"status":"public","title":"Additional file 1: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes","oa":1,"user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","publisher":"Springer Nature","date_updated":"2023-09-13T09:10:47Z","doi":"10.6084/m9.figshare.7295339.v1","type":"research_data_reference","date_published":"2018-11-03T00:00:00Z","_id":"9807","year":"2018","department":[{"_id":"SiHi"}],"day":"03","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)."}],"fulldoi":"https://doi.org/10.6084/m9.figshare.7295339.v1","related_material":{"record":[{"relation":"used_in_publication","status":"public","id":"20"}]},"date_created":"2021-08-06T12:26:53Z","author":[{"last_name":"Higareda Almaraz","full_name":"Higareda Almaraz, Juan","first_name":"Juan"},{"first_name":"Michael","last_name":"Karbiener","full_name":"Karbiener, Michael"},{"first_name":"Maude","full_name":"Giroud, Maude","last_name":"Giroud"},{"orcid":"0000-0002-7462-0048","first_name":"Florian","full_name":"Pauler, Florian","last_name":"Pauler","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Teresa","full_name":"Gerhalter, Teresa","last_name":"Gerhalter"},{"first_name":"Stephan","last_name":"Herzig","full_name":"Herzig, Stephan"},{"first_name":"Marcel","last_name":"Scheideler","full_name":"Scheideler, Marcel"}],"main_file_link":[{"url":"https://doi.org/10.6084/m9.figshare.7295339.v1","open_access":"1"}]},{"author":[{"full_name":"Higareda Almaraz, Juan","last_name":"Higareda Almaraz","first_name":"Juan"},{"first_name":"Michael","full_name":"Karbiener, Michael","last_name":"Karbiener"},{"first_name":"Maude","full_name":"Giroud, Maude","last_name":"Giroud"},{"orcid":"0000-0002-7462-0048","first_name":"Florian","full_name":"Pauler, Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","last_name":"Pauler"},{"last_name":"Gerhalter","full_name":"Gerhalter, Teresa","first_name":"Teresa"},{"full_name":"Herzig, Stephan","last_name":"Herzig","first_name":"Stephan"},{"first_name":"Marcel","full_name":"Scheideler, Marcel","last_name":"Scheideler"}],"main_file_link":[{"url":"https://doi.org/10.6084/m9.figshare.7295369.v1","open_access":"1"}],"day":"03","oa_version":"Published Version","abstract":[{"text":"Table S4. Counts per Gene per Million Reads Mapped. (XLSX 2751 kb).","lang":"eng"}],"fulldoi":"https://doi.org/10.6084/m9.figshare.7295369.v1","related_material":{"record":[{"id":"20","relation":"used_in_publication","status":"public"}]},"date_created":"2021-08-06T12:31:57Z","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","publisher":"Springer Nature","date_updated":"2023-09-13T09:10:47Z","doi":"10.6084/m9.figshare.7295369.v1","date_published":"2018-11-03T00:00:00Z","type":"research_data_reference","_id":"9808","year":"2018","department":[{"_id":"SiHi"}],"month":"11","article_processing_charge":"No","status":"public","citation":{"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, <a href=\"https://doi.org/10.6084/m9.figshare.7295369.v1\">10.6084/m9.figshare.7295369.v1</a>.","apa":"Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T., Herzig, S., &#38; Scheideler, M. (2018). Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. Springer Nature. <a href=\"https://doi.org/10.6084/m9.figshare.7295369.v1\">https://doi.org/10.6084/m9.figshare.7295369.v1</a>","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. <a href=\"https://doi.org/10.6084/m9.figshare.7295369.v1\">https://doi.org/10.6084/m9.figshare.7295369.v1</a>.","short":"J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S. Herzig, M. Scheideler, (2018).","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:<a href=\"https://doi.org/10.6084/m9.figshare.7295369.v1\">10.6084/m9.figshare.7295369.v1</a>","ieee":"J. Higareda Almaraz <i>et al.</i>, “Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes.” Springer Nature, 2018.","mla":"Higareda Almaraz, Juan, et al. <i>Additional File 3: Of Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes</i>. Springer Nature, 2018, doi:<a href=\"https://doi.org/10.6084/m9.figshare.7295369.v1\">10.6084/m9.figshare.7295369.v1</a>."},"title":"Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes","oa":1},{"date_created":"2020-09-21T12:01:50Z","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.","das_tickbox":"1","fulldoi":"https://doi.org/10.1101/494088","abstract":[{"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.","lang":"eng"}],"oa_version":"Preprint","day":"13","main_file_link":[{"url":"https://doi.org/10.1101/494088","open_access":"1"}],"author":[{"first_name":"Alfredo","last_name":"Llorca","full_name":"Llorca, Alfredo"},{"first_name":"Gabriele","last_name":"Ciceri","full_name":"Ciceri, Gabriele"},{"orcid":"0000-0002-8483-8753","first_name":"Robert J","full_name":"Beattie, Robert J","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","last_name":"Beattie"},{"last_name":"Wong","full_name":"Wong, Fong K.","first_name":"Fong K."},{"last_name":"Diana","full_name":"Diana, Giovanni","first_name":"Giovanni"},{"last_name":"Serafeimidou","full_name":"Serafeimidou, Eleni","first_name":"Eleni"},{"full_name":"Fernández-Otero, Marian","last_name":"Fernández-Otero","first_name":"Marian"},{"last_name":"Streicher","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","full_name":"Streicher, Carmen","first_name":"Carmen"},{"first_name":"Sebastian J.","full_name":"Arnold, Sebastian J.","last_name":"Arnold"},{"last_name":"Meyer","full_name":"Meyer, Martin","first_name":"Martin"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","first_name":"Simon","orcid":"0000-0003-2279-1061"},{"first_name":"Miguel","full_name":"Maravall, Miguel","last_name":"Maravall"},{"last_name":"Marín","full_name":"Marín, Oscar","first_name":"Oscar"}],"oa":1,"title":"Heterogeneous progenitor cell behaviors underlie the assembly of neocortical cytoarchitecture","status":"public","citation":{"mla":"Llorca, Alfredo, et al. “Heterogeneous Progenitor Cell Behaviors Underlie the Assembly of Neocortical Cytoarchitecture.” <i>BioRxiv</i>, doi:<a href=\"https://doi.org/10.1101/494088\">10.1101/494088</a>.","ieee":"A. Llorca <i>et al.</i>, “Heterogeneous progenitor cell behaviors underlie the assembly of neocortical cytoarchitecture,” <i>bioRxiv</i>. .","ama":"Llorca A, Ciceri G, Beattie RJ, et al. Heterogeneous progenitor cell behaviors underlie the assembly of neocortical cytoarchitecture. <i>bioRxiv</i>. doi:<a href=\"https://doi.org/10.1101/494088\">10.1101/494088</a>","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.” <i>BioRxiv</i>, n.d. <a href=\"https://doi.org/10.1101/494088\">https://doi.org/10.1101/494088</a>.","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.).","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. <i>bioRxiv</i>. <a href=\"https://doi.org/10.1101/494088\">https://doi.org/10.1101/494088</a>","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, <a href=\"https://doi.org/10.1101/494088\">10.1101/494088</a>."},"article_processing_charge":"No","publication":"bioRxiv","month":"12","project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780","call_identifier":"H2020"},{"_id":"264E56E2-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"M02416","name":"Molecular Mechanisms Regulating Gliogenesis in the Neocortex"}],"year":"2018","department":[{"_id":"SiHi"}],"_id":"8547","type":"preprint","date_published":"2018-12-13T00:00:00Z","ec_funded":1,"doi":"10.1101/494088","date_updated":"2026-07-06T12:52:50Z","language":[{"iso":"eng"}],"publication_status":"submitted","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87"},{"external_id":{"isi":["000446548100012"]},"day":"01","oa_version":"None","intvolume":"       141","publisher":"Oxford University Press","doi":"10.1093/brain/awy218","publication_status":"published","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","language":[{"iso":"eng"}],"department":[{"_id":"SiHi"}],"year":"2018","issue":"9","isi":1,"type":"journal_article","publication":"Brain a journal of neurology","article_processing_charge":"No","citation":{"ista":"Contreras X, Hippenmeyer S. 2018. Incorrect trafficking route leads to autism. Brain a journal of neurology. 141(9), 2542–2544.","chicago":"Contreras, Ximena, and Simon Hippenmeyer. “Incorrect Trafficking Route Leads to Autism.” <i>Brain a Journal of Neurology</i>. Oxford University Press, 2018. <a href=\"https://doi.org/10.1093/brain/awy218\">https://doi.org/10.1093/brain/awy218</a>.","short":"X. Contreras, S. Hippenmeyer, Brain a Journal of Neurology 141 (2018) 2542–2544.","apa":"Contreras, X., &#38; Hippenmeyer, S. (2018). Incorrect trafficking route leads to autism. <i>Brain a Journal of Neurology</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/brain/awy218\">https://doi.org/10.1093/brain/awy218</a>","ieee":"X. Contreras and S. Hippenmeyer, “Incorrect trafficking route leads to autism,” <i>Brain a journal of neurology</i>, vol. 141, no. 9. Oxford University Press, pp. 2542–2544, 2018.","ama":"Contreras X, Hippenmeyer S. Incorrect trafficking route leads to autism. <i>Brain a journal of neurology</i>. 2018;141(9):2542-2544. doi:<a href=\"https://doi.org/10.1093/brain/awy218\">10.1093/brain/awy218</a>","mla":"Contreras, Ximena, and Simon Hippenmeyer. “Incorrect Trafficking Route Leads to Autism.” <i>Brain a Journal of Neurology</i>, vol. 141, no. 9, Oxford University Press, 2018, pp. 2542–44, doi:<a href=\"https://doi.org/10.1093/brain/awy218\">10.1093/brain/awy218</a>."},"author":[{"full_name":"Contreras, Ximena","id":"475990FE-F248-11E8-B48F-1D18A9856A87","last_name":"Contreras","first_name":"Ximena"},{"orcid":"0000-0003-2279-1061","first_name":"Simon","full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer"}],"fulldoi":"https://doi.org/10.1093/brain/awy218","related_material":{"record":[{"relation":"part_of_dissertation","status":"public","id":"7902"}]},"abstract":[{"lang":"eng","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. "}],"date_created":"2018-12-11T11:44:14Z","quality_controlled":"1","date_updated":"2026-09-11T22:30:21Z","_id":"28","scopus_import":"1","date_published":"2018-09-01T00:00:00Z","month":"09","page":"2542 - 2544","volume":141,"status":"public","title":"Incorrect trafficking route leads to autism"},{"supervisor":[{"full_name":"Vicoso, Beatriz","id":"49E1C5C6-F248-11E8-B48F-1D18A9856A87","last_name":"Vicoso","orcid":"0000-0002-4579-8306","first_name":"Beatriz"}],"oa_version":"Published Version","day":"21","department":[{"_id":"SiHi"},{"_id":"GradSch"}],"year":"2018","type":"dissertation","publisher":"Institute of Science and Technology Austria","doi":"10.15479/AT:ISTA:th1057","alternative_title":["ISTA Thesis"],"language":[{"iso":"eng"}],"user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","publication_status":"published","citation":{"ista":"Laukoter S. 2018. Role of genomic imprinting in cerebral cortex development. Institute of Science and Technology Austria.","mla":"Laukoter, Susanne. <i>Role of Genomic Imprinting in Cerebral Cortex Development</i>. Institute of Science and Technology Austria, 2018, pp. 1–139, doi:<a href=\"https://doi.org/10.15479/AT:ISTA:th1057\">10.15479/AT:ISTA:th1057</a>.","chicago":"Laukoter, Susanne. “Role of Genomic Imprinting in Cerebral Cortex Development.” Institute of Science and Technology Austria, 2018. <a href=\"https://doi.org/10.15479/AT:ISTA:th1057\">https://doi.org/10.15479/AT:ISTA:th1057</a>.","apa":"Laukoter, S. (2018). <i>Role of genomic imprinting in cerebral cortex development</i>. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/AT:ISTA:th1057\">https://doi.org/10.15479/AT:ISTA:th1057</a>","short":"S. Laukoter, Role of Genomic Imprinting in Cerebral Cortex Development, Institute of Science and Technology Austria, 2018.","ama":"Laukoter S. Role of genomic imprinting in cerebral cortex development. 2018:1-139. doi:<a href=\"https://doi.org/10.15479/AT:ISTA:th1057\">10.15479/AT:ISTA:th1057</a>","ieee":"S. Laukoter, “Role of genomic imprinting in cerebral cortex development,” Institute of Science and Technology Austria, 2018."},"article_processing_charge":"No","has_accepted_license":"1","ddc":["570"],"author":[{"orcid":"0000-0002-7903-3010","first_name":"Susanne","full_name":"Laukoter, Susanne","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","last_name":"Laukoter"}],"degree_awarded":"PhD","date_created":"2018-12-11T11:44:08Z","OA_place":"publisher","file":[{"date_updated":"2019-11-23T23:30:03Z","checksum":"41fdbf5fdce312802935d88a8ad9932c","file_size":17949175,"embargo_to":"open_access","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","creator":"dernst","file_id":"6396","access_level":"closed","date_created":"2019-05-10T07:47:04Z","relation":"source_file","file_name":"Thesis_LaukoterSusanne_FINAL.docx"},{"file_size":21187245,"checksum":"53001a9a0c9e570e598d861bb0af28aa","date_updated":"2021-02-11T11:17:16Z","relation":"main_file","file_name":"Thesis_LaukoterSusanne_FINAL.pdf","embargo":"2019-11-21","date_created":"2019-05-10T07:47:04Z","content_type":"application/pdf","creator":"dernst","file_id":"6397","access_level":"open_access"}],"fulldoi":"https://doi.org/10.15479/AT:ISTA:th1057","doi_confirm":"1","publication_identifier":{"issn":["2663-337X"]},"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"}],"_id":"10","publist_id":"8046","date_published":"2018-11-21T00:00:00Z","corr_author":"1","date_updated":"2026-07-29T13:40:27Z","oa":1,"pubrep_id":"1057","page":"1 - 139","file_date_updated":"2021-02-11T11:17:16Z","status":"public","title":"Role of genomic imprinting in cerebral cortex development","month":"11"},{"author":[{"orcid":"0000-0002-8483-8753","first_name":"Robert J","full_name":"Beattie, Robert J","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","last_name":"Beattie"},{"orcid":"0000-0003-2279-1061","first_name":"Simon","full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer"}],"pmid":1,"ddc":["571","610"],"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."}],"publication_identifier":{"issn":["0014-5793"]},"file":[{"checksum":"a46dadc84e0c28d389dd3e9e954464db","file_size":644149,"date_updated":"2020-07-14T12:47:24Z","date_created":"2018-12-12T10:16:24Z","relation":"main_file","file_name":"IST-2018-928-v1+1_Beattie_et_al-2017-FEBS_Letters.pdf","creator":"system","content_type":"application/pdf","access_level":"open_access","file_id":"5211"}],"fulldoi":"https://doi.org/10.1002/1873-3468.12906","date_created":"2018-12-11T11:47:32Z","date_updated":"2025-09-11T07:31:36Z","quality_controlled":"1","corr_author":"1","date_published":"2017-12-01T00:00:00Z","publist_id":"7183","scopus_import":"1","_id":"621","month":"12","project":[{"name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level","_id":"25D7962E-B435-11E9-9278-68D0E5697425","grant_number":"RGP0053/2014"},{"name":"Molecular Mechanisms of Cerebral Cortex Development","grant_number":"618444","call_identifier":"FP7","_id":"25D61E48-B435-11E9-9278-68D0E5697425"}],"title":"Mechanisms of radial glia progenitor cell lineage progression","volume":591,"status":"public","file_date_updated":"2020-07-14T12:47:24Z","page":"3993  - 4008","pubrep_id":"928","oa":1,"external_id":{"isi":["000418825700004"],"pmid":["29121403"]},"oa_version":"Published Version","day":"01","intvolume":"       591","language":[{"iso":"eng"}],"publication_status":"published","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","ec_funded":1,"doi":"10.1002/1873-3468.12906","publisher":"Wiley-Blackwell","type":"journal_article","isi":1,"department":[{"_id":"SiHi"}],"issue":"24","year":"2017","has_accepted_license":"1","article_processing_charge":"Yes (in subscription journal)","tmp":{"short":"CC BY-NC (4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc/4.0/legalcode","name":"Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)","image":"/images/cc_by_nc.png"},"publication":"FEBS letters","citation":{"ista":"Beattie RJ, Hippenmeyer S. 2017. Mechanisms of radial glia progenitor cell lineage progression. FEBS letters. 591(24), 3993–4008.","mla":"Beattie, Robert J., and Simon Hippenmeyer. “Mechanisms of Radial Glia Progenitor Cell Lineage Progression.” <i>FEBS Letters</i>, vol. 591, no. 24, Wiley-Blackwell, 2017, pp. 3993–4008, doi:<a href=\"https://doi.org/10.1002/1873-3468.12906\">10.1002/1873-3468.12906</a>.","apa":"Beattie, R. J., &#38; Hippenmeyer, S. (2017). Mechanisms of radial glia progenitor cell lineage progression. <i>FEBS Letters</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1002/1873-3468.12906\">https://doi.org/10.1002/1873-3468.12906</a>","chicago":"Beattie, Robert J, and Simon Hippenmeyer. “Mechanisms of Radial Glia Progenitor Cell Lineage Progression.” <i>FEBS Letters</i>. Wiley-Blackwell, 2017. <a href=\"https://doi.org/10.1002/1873-3468.12906\">https://doi.org/10.1002/1873-3468.12906</a>.","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,” <i>FEBS letters</i>, vol. 591, no. 24. Wiley-Blackwell, pp. 3993–4008, 2017.","ama":"Beattie RJ, Hippenmeyer S. Mechanisms of radial glia progenitor cell lineage progression. <i>FEBS letters</i>. 2017;591(24):3993-4008. doi:<a href=\"https://doi.org/10.1002/1873-3468.12906\">10.1002/1873-3468.12906</a>"}},{"title":"Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability","status":"public","volume":26,"page":"258 - 269","month":"01","date_published":"2017-01-01T00:00:00Z","scopus_import":"1","publist_id":"6379","_id":"1016","date_updated":"2026-04-16T09:56:51Z","quality_controlled":"1","date_created":"2018-12-11T11:49:42Z","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."}],"publication_identifier":{"issn":["0964-6906"]},"fulldoi":"https://doi.org/10.1093/hmg/ddw383","author":[{"first_name":"Martin","full_name":"Breuss, Martin","last_name":"Breuss"},{"first_name":"Thai","last_name":"Nguyen","full_name":"Nguyen, Thai"},{"full_name":"Srivatsan, Anjana","last_name":"Srivatsan","first_name":"Anjana"},{"last_name":"Leca","full_name":"Leca, Ines","first_name":"Ines"},{"first_name":"Guoling","full_name":"Tian, Guoling","last_name":"Tian"},{"first_name":"Tanja","last_name":"Fritz","full_name":"Fritz, Tanja"},{"full_name":"Hansen, Andi H","last_name":"Hansen","id":"38853E16-F248-11E8-B48F-1D18A9856A87","first_name":"Andi H"},{"first_name":"Damir","full_name":"Musaev, Damir","last_name":"Musaev"},{"first_name":"Jennifer","last_name":"Mcevoy Venneri","full_name":"Mcevoy Venneri, Jennifer"},{"full_name":"Kiely, James","last_name":"Kiely","first_name":"James"},{"full_name":"Rosti, Rasim","last_name":"Rosti","first_name":"Rasim"},{"full_name":"Scott, Eric","last_name":"Scott","first_name":"Eric"},{"last_name":"Tan","full_name":"Tan, Uner","first_name":"Uner"},{"full_name":"Kolodner, Richard","last_name":"Kolodner","first_name":"Richard"},{"full_name":"Cowan, Nicholas","last_name":"Cowan","first_name":"Nicholas"},{"first_name":"David","full_name":"Keays, David","last_name":"Keays"},{"last_name":"Gleeson","full_name":"Gleeson, Joseph","first_name":"Joseph"}],"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.","mla":"Breuss, Martin, et al. “Uner Tan Syndrome Caused by a Homozygous TUBB2B Mutation Affecting Microtubule Stability.” <i>Human Molecular Genetics</i>, vol. 26, no. 2, Oxford University Press, 2017, pp. 258–69, doi:<a href=\"https://doi.org/10.1093/hmg/ddw383\">10.1093/hmg/ddw383</a>.","ama":"Breuss M, Nguyen T, Srivatsan A, et al. Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability. <i>Human Molecular Genetics</i>. 2017;26(2):258-269. doi:<a href=\"https://doi.org/10.1093/hmg/ddw383\">10.1093/hmg/ddw383</a>","ieee":"M. Breuss <i>et al.</i>, “Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability,” <i>Human Molecular Genetics</i>, vol. 26, no. 2. Oxford University Press, pp. 258–269, 2017.","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. <i>Human Molecular Genetics</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/hmg/ddw383\">https://doi.org/10.1093/hmg/ddw383</a>","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.” <i>Human Molecular Genetics</i>. Oxford University Press, 2017. <a href=\"https://doi.org/10.1093/hmg/ddw383\">https://doi.org/10.1093/hmg/ddw383</a>.","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."},"article_processing_charge":"No","publication":"Human Molecular Genetics","type":"journal_article","isi":1,"department":[{"_id":"SiHi"}],"year":"2017","issue":"2","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","language":[{"iso":"eng"}],"publication_status":"published","doi":"10.1093/hmg/ddw383","publisher":"Oxford University Press","intvolume":"        26","oa_version":"None","day":"01","external_id":{"isi":["000397066400002"]}},{"external_id":{"isi":["000415140700007"]},"day":"01","oa_version":"Published Version","intvolume":"        84","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","language":[{"iso":"eng"}],"publication_status":"published","publisher":"Academic Press","doi":"10.1016/j.mcn.2017.03.002","isi":1,"type":"journal_article","department":[{"_id":"SiHi"}],"year":"2017","has_accepted_license":"1","publication":"Molecular and Cellular Neuroscience","article_processing_charge":"No","tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","image":"/images/cc_by_nc_nd.png","short":"CC BY-NC-ND (4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"citation":{"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.","mla":"Breuss, Martin, et al. “Tubulins and Brain Development: The Origins of Functional Specification.” <i>Molecular and Cellular Neuroscience</i>, vol. 84, Academic Press, 2017, pp. 58–67, doi:<a href=\"https://doi.org/10.1016/j.mcn.2017.03.002\">10.1016/j.mcn.2017.03.002</a>.","chicago":"Breuss, Martin, Ines Leca, Thomas Gstrein, Andi H Hansen, and David Keays. “Tubulins and Brain Development: The Origins of Functional Specification.” <i>Molecular and Cellular Neuroscience</i>. Academic Press, 2017. <a href=\"https://doi.org/10.1016/j.mcn.2017.03.002\">https://doi.org/10.1016/j.mcn.2017.03.002</a>.","short":"M. Breuss, I. Leca, T. Gstrein, A.H. Hansen, D. Keays, Molecular and Cellular Neuroscience 84 (2017) 58–67.","apa":"Breuss, M., Leca, I., Gstrein, T., Hansen, A. H., &#38; Keays, D. (2017). Tubulins and brain development: The origins of functional specification. <i>Molecular and Cellular Neuroscience</i>. Academic Press. <a href=\"https://doi.org/10.1016/j.mcn.2017.03.002\">https://doi.org/10.1016/j.mcn.2017.03.002</a>","ieee":"M. Breuss, I. Leca, T. Gstrein, A. H. Hansen, and D. Keays, “Tubulins and brain development: The origins of functional specification,” <i>Molecular and Cellular Neuroscience</i>, vol. 84. Academic Press, pp. 58–67, 2017.","ama":"Breuss M, Leca I, Gstrein T, Hansen AH, Keays D. Tubulins and brain development: The origins of functional specification. <i>Molecular and Cellular Neuroscience</i>. 2017;84:58-67. doi:<a href=\"https://doi.org/10.1016/j.mcn.2017.03.002\">10.1016/j.mcn.2017.03.002</a>"},"author":[{"last_name":"Breuss","full_name":"Breuss, Martin","first_name":"Martin"},{"last_name":"Leca","full_name":"Leca, Ines","first_name":"Ines"},{"full_name":"Gstrein, Thomas","last_name":"Gstrein","first_name":"Thomas"},{"first_name":"Andi H","full_name":"Hansen, Andi H","last_name":"Hansen","id":"38853E16-F248-11E8-B48F-1D18A9856A87"},{"first_name":"David","last_name":"Keays","full_name":"Keays, David"}],"ddc":["571"],"publication_identifier":{"issn":["1044-7431"]},"abstract":[{"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.","lang":"eng"}],"fulldoi":"https://doi.org/10.1016/j.mcn.2017.03.002","file":[{"date_created":"2018-12-12T10:09:19Z","relation":"main_file","file_name":"IST-2017-806-v1+2_1-s2.0-S1044743116302500-main_1_.pdf","content_type":"application/pdf","creator":"system","access_level":"open_access","file_id":"4742","file_size":1436377,"date_updated":"2018-12-12T10:09:19Z"}],"date_created":"2018-12-11T11:49:42Z","quality_controlled":"1","date_updated":"2025-07-10T11:49:44Z","publist_id":"6377","scopus_import":"1","date_published":"2017-10-01T00:00:00Z","_id":"1017","month":"10","volume":84,"status":"public","title":"Tubulins and brain development: The origins of functional specification","oa":1,"page":"58 - 67","file_date_updated":"2018-12-12T10:09:19Z","pubrep_id":"806"}]