[{"article_number":"104942","department":[{"_id":"SiHi"}],"date_created":"2025-07-27T22:01:25Z","publication_identifier":{"eissn":["1472-6491"],"issn":["1472-6483"]},"intvolume":"        51","language":[{"iso":"eng"}],"quality_controlled":"1","external_id":{"isi":["001549819000002"],"pmid":["40680553"]},"date_updated":"2025-09-30T14:10:46Z","publication":"Reproductive Biomedicine Online","volume":51,"citation":{"short":"I. Yotova, K. Proestling, F. Pauler, L. Rainer, L. Kaup, J. Heine, L. Sandrieser, R. Wenzl, Q.J. Hudson, Reproductive Biomedicine Online 51 (2025).","ieee":"I. Yotova <i>et al.</i>, “LINC01638 promotes epithelial-to-mesenchymal transition in endometriosis epithelial cells by up-regulating RHOB via HDAC1 suppression,” <i>Reproductive Biomedicine Online</i>, vol. 51, no. 3. Elsevier, 2025.","apa":"Yotova, I., Proestling, K., Pauler, F., Rainer, L., Kaup, L., Heine, J., … Hudson, Q. J. (2025). LINC01638 promotes epithelial-to-mesenchymal transition in endometriosis epithelial cells by up-regulating RHOB via HDAC1 suppression. <i>Reproductive Biomedicine Online</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.rbmo.2025.104942\">https://doi.org/10.1016/j.rbmo.2025.104942</a>","mla":"Yotova, Iveta, et al. “LINC01638 Promotes Epithelial-to-Mesenchymal Transition in Endometriosis Epithelial Cells by up-Regulating RHOB via HDAC1 Suppression.” <i>Reproductive Biomedicine Online</i>, vol. 51, no. 3, 104942, Elsevier, 2025, doi:<a href=\"https://doi.org/10.1016/j.rbmo.2025.104942\">10.1016/j.rbmo.2025.104942</a>.","ista":"Yotova I, Proestling K, Pauler F, Rainer L, Kaup L, Heine J, Sandrieser L, Wenzl R, Hudson QJ. 2025. LINC01638 promotes epithelial-to-mesenchymal transition in endometriosis epithelial cells by up-regulating RHOB via HDAC1 suppression. Reproductive Biomedicine Online. 51(3), 104942.","ama":"Yotova I, Proestling K, Pauler F, et al. LINC01638 promotes epithelial-to-mesenchymal transition in endometriosis epithelial cells by up-regulating RHOB via HDAC1 suppression. <i>Reproductive Biomedicine Online</i>. 2025;51(3). doi:<a href=\"https://doi.org/10.1016/j.rbmo.2025.104942\">10.1016/j.rbmo.2025.104942</a>","chicago":"Yotova, Iveta, Katharina Proestling, Florian Pauler, Lisa Rainer, Leonie Kaup, Jana Heine, Lejla Sandrieser, René Wenzl, and Quanah J. Hudson. “LINC01638 Promotes Epithelial-to-Mesenchymal Transition in Endometriosis Epithelial Cells by up-Regulating RHOB via HDAC1 Suppression.” <i>Reproductive Biomedicine Online</i>. Elsevier, 2025. <a href=\"https://doi.org/10.1016/j.rbmo.2025.104942\">https://doi.org/10.1016/j.rbmo.2025.104942</a>."},"type":"journal_article","day":"17","publisher":"Elsevier","doi":"10.1016/j.rbmo.2025.104942","author":[{"first_name":"Iveta","full_name":"Yotova, Iveta","last_name":"Yotova"},{"full_name":"Proestling, Katharina","first_name":"Katharina","last_name":"Proestling"},{"id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","first_name":"Florian","last_name":"Pauler","orcid":"0000-0002-7462-0048"},{"first_name":"Lisa","full_name":"Rainer, Lisa","last_name":"Rainer"},{"first_name":"Leonie","full_name":"Kaup, Leonie","last_name":"Kaup"},{"last_name":"Heine","first_name":"Jana","full_name":"Heine, Jana"},{"first_name":"Lejla","full_name":"Sandrieser, Lejla","last_name":"Sandrieser"},{"last_name":"Wenzl","first_name":"René","full_name":"Wenzl, René"},{"full_name":"Hudson, Quanah J.","first_name":"Quanah J.","last_name":"Hudson"}],"article_type":"original","publication_status":"published","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","isi":1,"status":"public","scopus_import":"1","date_published":"2025-07-17T00:00:00Z","abstract":[{"lang":"eng","text":"Research question: Is LINC01638 involved in regulation of epithelial-to-mesenchymal transition (EMT) in endometriosis?\r\nDesign: A prospective patient cohort study was combined with functional experiments in the 12Z endometriosis epithelial cell line to investigate the role of LINC01638 in endometriosis. Eutopic endometrial samples were collected by curettage, and ectopic endometrial lesion samples were collected by laparoscopic surgery from 24 control patients and 41 patients with endometriosis. The phenotype of 12Z cells was assessed following LINC01638 knockdown using siRNA, performing proliferation, adhesion, migration and invasion assays, as well as assessing apoptosis and cell cycle changes with flow cytometry assays. In order to assess the relationship between LINC01638 and histone deacetylase class 1 enzyme (HDAC1), LINC01638 knockdown was combined with HDAC inhibition with the specific HDAC inhibitor romidepsin.\r\nResults: LINC01638 was up-regulated in the epithelial layer of endometriotic lesions, and LINC01638 knockdown in 12Z cells led to reduced proliferation, adhesion, migration and invasion. The reduction in proliferation was associated with increased p21 and p27 expression, and G1 phase arrest. Further analysis of LINC01638 control and knockdown cells revealed that a number of transcription factors associated with EMT are down-regulated in knockdown cells, along with the cytoskeleton regulatory gene RHOB, while HDAC1 was up-regulated. Chromatin immunoprecipitation analysis and HDAC1 inhibitory treatment combined with LINC01638 knockdown indicated that LINC01638 regulates RHOB expression via HDAC1-mediated promoter deacetylation. RHOB is up-regulated in the epithelial layer of endometriotic lesions compared with eutopic endometrium, supporting a role in the disease.\r\nConclusions: LINC01638 is an epigenetic regulator of the pathogenesis of endometriosis, promoting proliferation and EMT of endometriotic lesions."}],"acknowledgement":"The authors wish to thank all the participants and health professionals involved in this study. In addition, the authors wish to thank technical assistants Barbara Widmar, Matthias Witzmann-Stern and Isabella Haslinger for their work assisting with this study; and Simon Hippenmeyer for access to bioinformatic infrastructure and resources.\r\nOpen access funding was provided by the Medical University of Vienna.","OA_type":"closed access","article_processing_charge":"No","month":"07","pmid":1,"oa_version":"None","year":"2025","issue":"3","_id":"20079","title":"LINC01638 promotes epithelial-to-mesenchymal transition in endometriosis epithelial cells by up-regulating RHOB via HDAC1 suppression"},{"title":"Probing Cell-Type Specificity of Mutant Phenotype at Transcriptomic Level Using Mosaic Analysis with Double Markers (MADM)","_id":"18765","year":"2025","oa_version":"None","pmid":1,"month":"01","article_processing_charge":"No","alternative_title":["Methods in Molecular Biology"],"OA_type":"closed access","acknowledgement":"We thank all Hippenmeyer lab members for support and discussions. Experimental steps described were optimized with support provided by the Imaging & Optics Facility (IOF) and Preclinical Facility (PCF) at ISTA, Vienna BioCenter Core Facilities (VBCF), and Christoph Bock lab at Center for Molecular Medicine (CeMM). G.C. received funding from European Commission (IST plus postdoctoral fellowship). This work was supported by ISTA institutional funds: The Austrian Science Fund Special Research Programmes (FWF SFB F78 Neuro Stem Modulation) to S.H.","abstract":[{"text":"Mosaic Analysis with Double Markers (MADM) represents a mouse genetic approach coupling differential fluorescent labeling to genetic manipulations in dividing cells and their lineages. MADM uniquely enables the generation and visualization of individual control or homozygous mutant cells in a heterozygous genetic environment. Among its diverse applications, MADM has been used to dissect cell-autonomous gene functions important for cortical development and neural development in general. The high cellular resolution offered by MADM also permits the analysis of transcriptomic changes of individual cells upon genetic manipulations. In this chapter, we describe an experimental protocol combining the generation and isolation of MADM-labeled cells with downstream single-cell RNA-sequencing technologies to probe cell-type specific phenotypes due to genetic mutations at single-cell resolution.","lang":"eng"}],"scopus_import":"1","date_published":"2025-01-03T00:00:00Z","status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_status":"published","project":[{"name":"ISTplus - Postdoctoral Fellowships","call_identifier":"H2020","_id":"260C2330-B435-11E9-9278-68D0E5697425","grant_number":"754411"}],"author":[{"last_name":"Cheung","orcid":"0000-0001-8457-2572","first_name":"Giselle T","full_name":"Cheung, Giselle T","id":"471195F6-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Pauler","orcid":"0000-0002-7462-0048","first_name":"Florian","full_name":"Pauler, Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061"}],"doi":"10.1007/978-1-0716-4310-5_7","publisher":"Springer Nature","day":"03","page":"139-151","ec_funded":1,"type":"book_chapter","citation":{"short":"G.T. Cheung, F. Pauler, S. Hippenmeyer, in:, J. Garcia-Marques, T. Lee (Eds.), Lineage Tracing, Springer Nature, New York, NY, 2025, pp. 139–151.","ista":"Cheung GT, Pauler F, Hippenmeyer S. 2025.Probing Cell-Type Specificity of Mutant Phenotype at Transcriptomic Level Using Mosaic Analysis with Double Markers (MADM). In: Lineage Tracing. Methods in Molecular Biology, vol. 2886, 139–151.","apa":"Cheung, G. T., Pauler, F., &#38; Hippenmeyer, S. (2025). Probing Cell-Type Specificity of Mutant Phenotype at Transcriptomic Level Using Mosaic Analysis with Double Markers (MADM). In J. Garcia-Marques &#38; T. Lee (Eds.), <i>Lineage Tracing</i> (Vol. 2886, pp. 139–151). New York, NY: Springer Nature. <a href=\"https://doi.org/10.1007/978-1-0716-4310-5_7\">https://doi.org/10.1007/978-1-0716-4310-5_7</a>","mla":"Cheung, Giselle T., et al. “Probing Cell-Type Specificity of Mutant Phenotype at Transcriptomic Level Using Mosaic Analysis with Double Markers (MADM).” <i>Lineage Tracing</i>, edited by Jorge Garcia-Marques and Tzumin Lee, vol. 2886, Springer Nature, 2025, pp. 139–51, doi:<a href=\"https://doi.org/10.1007/978-1-0716-4310-5_7\">10.1007/978-1-0716-4310-5_7</a>.","ieee":"G. T. Cheung, F. Pauler, and S. Hippenmeyer, “Probing Cell-Type Specificity of Mutant Phenotype at Transcriptomic Level Using Mosaic Analysis with Double Markers (MADM),” in <i>Lineage Tracing</i>, vol. 2886, J. Garcia-Marques and T. Lee, Eds. New York, NY: Springer Nature, 2025, pp. 139–151.","ama":"Cheung GT, Pauler F, Hippenmeyer S. Probing Cell-Type Specificity of Mutant Phenotype at Transcriptomic Level Using Mosaic Analysis with Double Markers (MADM). In: Garcia-Marques J, Lee T, eds. <i>Lineage Tracing</i>. Vol 2886. MIMB. New York, NY: Springer Nature; 2025:139-151. doi:<a href=\"https://doi.org/10.1007/978-1-0716-4310-5_7\">10.1007/978-1-0716-4310-5_7</a>","chicago":"Cheung, Giselle T, Florian Pauler, and Simon Hippenmeyer. “Probing Cell-Type Specificity of Mutant Phenotype at Transcriptomic Level Using Mosaic Analysis with Double Markers (MADM).” In <i>Lineage Tracing</i>, edited by Jorge Garcia-Marques and Tzumin Lee, 2886:139–51. MIMB. New York, NY: Springer Nature, 2025. <a href=\"https://doi.org/10.1007/978-1-0716-4310-5_7\">https://doi.org/10.1007/978-1-0716-4310-5_7</a>."},"volume":2886,"place":"New York, NY","publication":"Lineage Tracing","editor":[{"first_name":"Jorge","full_name":"Garcia-Marques, Jorge","last_name":"Garcia-Marques"},{"last_name":"Lee","full_name":"Lee, Tzumin","first_name":"Tzumin"}],"date_updated":"2025-04-14T07:43:46Z","corr_author":"1","external_id":{"pmid":["39745639"]},"language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"      2886","publication_identifier":{"eissn":["1940-6029"],"issn":["1064-3745"],"eisbn":["9781071643105"],"isbn":["9781071643099"]},"acknowledged_ssus":[{"_id":"Bio"}],"date_created":"2025-01-07T08:36:47Z","department":[{"_id":"SiHi"}],"series_title":"MIMB"},{"oa":1,"file":[{"file_name":"2024_Neuron_Cheung.pdf","date_updated":"2024-02-06T13:56:15Z","checksum":"32b3788f7085cf44a84108d8faaff3ce","success":1,"relation":"main_file","file_size":5942467,"file_id":"14944","creator":"dernst","date_created":"2024-02-06T13:56:15Z","access_level":"open_access","content_type":"application/pdf"}],"isi":1,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"first_name":"Giselle T","id":"471195F6-F248-11E8-B48F-1D18A9856A87","full_name":"Cheung, Giselle T","orcid":"0000-0001-8457-2572","last_name":"Cheung"},{"id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","first_name":"Florian","orcid":"0000-0002-7462-0048","last_name":"Pauler"},{"first_name":"Peter","full_name":"Koppensteiner, Peter","id":"3B8B25A8-F248-11E8-B48F-1D18A9856A87","last_name":"Koppensteiner","orcid":"0000-0002-3509-1948"},{"full_name":"Krausgruber, Thomas","first_name":"Thomas","last_name":"Krausgruber"},{"first_name":"Carmen","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","full_name":"Streicher, Carmen","last_name":"Streicher"},{"last_name":"Schrammel","first_name":"Martin","id":"f13e7cae-e8bd-11ed-841a-96dedf69f46d","full_name":"Schrammel, Martin"},{"last_name":"Özgen","first_name":"Natalie Y","full_name":"Özgen, Natalie Y","id":"e68ece33-f6e0-11ea-865d-ae1031dcc090"},{"first_name":"Alexis","id":"1d144691-e8be-11ed-9b33-bdd3077fad4c","full_name":"Ivec, Alexis","last_name":"Ivec"},{"last_name":"Bock","full_name":"Bock, Christoph","first_name":"Christoph"},{"orcid":"0000-0001-8761-9444","last_name":"Shigemoto","first_name":"Ryuichi","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","full_name":"Shigemoto, Ryuichi"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"}],"project":[{"grant_number":"F7805","_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E","name":"Stem Cell Modulation in Neural Development and Regeneration/ P05-Molecular Mechanisms of Neural Stem Cell Lineage Progression"}],"publication_status":"published","article_type":"original","acknowledgement":"We thank Liqun Luo for his continued support, for providing essential resources for generating Fzd10-CreER mice which were generated in his laboratory, and for comments on the manuscript; W. Zhong for providing Nestin-Cre transgenic mouse line for this study; A. Heger for mouse colony management; R. Beattie and T. Asenov for designing and producing components of acute slice recovery chamber for MADM-CloneSeq experiments; and K. Leopold, J. Rodarte and N. Amberg for initial experiments, technical support and/or assistance. This study was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Imaging & Optics Facility (IOF), Laboratory Support Facility (LSF), Miba Machine Shop, and Pre-clinical Facility (PCF). G.C. received funding from European Commission (IST plus postdoctoral fellowship). This work was supported by ISTA institutional\r\nfunds; the Austrian Science Fund Special Research Programmes (FWF SFB F78 Neuro Stem Modulation) to S.H. ","ddc":["570"],"status":"public","date_published":"2024-01-17T00:00:00Z","scopus_import":"1","abstract":[{"text":"The superior colliculus (SC) in the mammalian midbrain is essential for multisensory integration and is composed of a rich diversity of excitatory and inhibitory neurons and glia. However, the developmental principles directing the generation of SC cell-type diversity are not understood. Here, we pursued systematic cell lineage tracing in silico and in vivo, preserving full spatial information, using genetic mosaic analysis with double markers (MADM)-based clonal analysis with single-cell sequencing (MADM-CloneSeq). The analysis of clonally related cell lineages revealed that radial glial progenitors (RGPs) in SC are exceptionally multipotent. Individual resident RGPs have the capacity to produce all excitatory and inhibitory SC neuron types, even at the stage of terminal division. While individual clonal units show no pre-defined cellular composition, the establishment of appropriate relative proportions of distinct neuronal types occurs in a PTEN-dependent manner. Collectively, our findings provide an inaugural framework at the single-RGP/-cell level of the mammalian SC ontogeny.","lang":"eng"}],"month":"01","pmid":1,"article_processing_charge":"Yes (via OA deal)","title":"Multipotent progenitors instruct ontogeny of the superior colliculus","oa_version":"Published Version","year":"2024","_id":"12875","issue":"2","acknowledged_ssus":[{"_id":"Bio"},{"_id":"M-Shop"},{"_id":"LifeSc"},{"_id":"PreCl"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"department":[{"_id":"SiHi"},{"_id":"RySh"}],"date_created":"2023-04-27T09:41:48Z","file_date_updated":"2024-02-06T13:56:15Z","external_id":{"pmid":["38096816"],"isi":["001163937900001"]},"corr_author":"1","date_updated":"2025-12-30T10:54:12Z","has_accepted_license":"1","publication_identifier":{"issn":["0896-6273"]},"intvolume":"       112","language":[{"iso":"eng"}],"quality_controlled":"1","publication":"Neuron","related_material":{"link":[{"url":"https://ista.ac.at/en/news/the-pedigree-of-brain-cells/","relation":"press_release","description":"News on ISTA Website"}]},"type":"journal_article","page":"230-246.e11","day":"17","doi":"10.1016/j.neuron.2023.11.009","publisher":"Elsevier","volume":112,"citation":{"chicago":"Cheung, Giselle T, Florian Pauler, Peter Koppensteiner, Thomas Krausgruber, Carmen Streicher, Martin Schrammel, Natalie Y Özgen, et al. “Multipotent Progenitors Instruct Ontogeny of the Superior Colliculus.” <i>Neuron</i>. Elsevier, 2024. <a href=\"https://doi.org/10.1016/j.neuron.2023.11.009\">https://doi.org/10.1016/j.neuron.2023.11.009</a>.","ama":"Cheung GT, Pauler F, Koppensteiner P, et al. Multipotent progenitors instruct ontogeny of the superior colliculus. <i>Neuron</i>. 2024;112(2):230-246.e11. doi:<a href=\"https://doi.org/10.1016/j.neuron.2023.11.009\">10.1016/j.neuron.2023.11.009</a>","ista":"Cheung GT, Pauler F, Koppensteiner P, Krausgruber T, Streicher C, Schrammel M, Özgen NY, Ivec A, Bock C, Shigemoto R, Hippenmeyer S. 2024. Multipotent progenitors instruct ontogeny of the superior colliculus. Neuron. 112(2), 230–246.e11.","apa":"Cheung, G. T., Pauler, F., Koppensteiner, P., Krausgruber, T., Streicher, C., Schrammel, M., … Hippenmeyer, S. (2024). Multipotent progenitors instruct ontogeny of the superior colliculus. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2023.11.009\">https://doi.org/10.1016/j.neuron.2023.11.009</a>","mla":"Cheung, Giselle T., et al. “Multipotent Progenitors Instruct Ontogeny of the Superior Colliculus.” <i>Neuron</i>, vol. 112, no. 2, Elsevier, 2024, p. 230–246.e11, doi:<a href=\"https://doi.org/10.1016/j.neuron.2023.11.009\">10.1016/j.neuron.2023.11.009</a>.","ieee":"G. T. Cheung <i>et al.</i>, “Multipotent progenitors instruct ontogeny of the superior colliculus,” <i>Neuron</i>, vol. 112, no. 2. Elsevier, p. 230–246.e11, 2024.","short":"G.T. Cheung, F. Pauler, P. Koppensteiner, T. Krausgruber, C. Streicher, M. Schrammel, N.Y. Özgen, A. Ivec, C. Bock, R. Shigemoto, S. Hippenmeyer, Neuron 112 (2024) 230–246.e11."}},{"article_processing_charge":"Yes","month":"09","pmid":1,"oa_version":"Published Version","year":"2024","issue":"3","_id":"17232","title":"Protocol for mapping cell lineage and cell-type identity of clonally-related cells in situ using MADM-CloneSeq","APC_amount":"804 EUR","author":[{"orcid":"0000-0001-8457-2572","last_name":"Cheung","first_name":"Giselle T","full_name":"Cheung, Giselle T","id":"471195F6-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","orcid":"0000-0002-7462-0048","last_name":"Pauler"},{"full_name":"Koppensteiner, Peter","id":"3B8B25A8-F248-11E8-B48F-1D18A9856A87","first_name":"Peter","last_name":"Koppensteiner","orcid":"0000-0002-3509-1948"},{"first_name":"Simon","full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"}],"license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","project":[{"grant_number":"F7805","_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E","name":"Stem Cell Modulation in Neural Development and Regeneration/ P05-Molecular Mechanisms of Neural Stem Cell Lineage Progression"}],"publication_status":"published","article_type":"original","oa":1,"file":[{"file_name":"2024_STARProtoc_Cheung2.pdf","date_updated":"2025-01-09T12:16:53Z","checksum":"464f52ecc6ec92f509552823bb82bf79","success":1,"relation":"main_file","file_size":6445556,"file_id":"18810","date_created":"2025-01-09T12:16:53Z","creator":"dernst","access_level":"open_access","content_type":"application/pdf"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","date_published":"2024-09-20T00:00:00Z","scopus_import":"1","abstract":[{"lang":"eng","text":"The lineage relationship of clonally-related cells offers important insights into the ontogeny and cytoarchitecture of the brain in health and disease. Here, we provide a protocol to concurrently assess cell lineage relationship and cell-type identity among clonally-related cells in situ. We first describe the preparation and screening of acute brain slices containing clonally-related cells labeled using mosaic analysis with double markers (MADM). We then outline steps to collect RNA from individual cells for downstream applications and cell-type identification using RNA sequencing.\r\nFor complete details on the use and execution of this protocol, please refer to Cheung et al.\r\n1"}],"acknowledgement":"We thank R. Beattie and T. Asenov for designing and producing components of the multi-well slice recover chamber. We thank R. Shigemoto for providing equipment access. We thank C. Streicher and A. Heger for mouse breeding support. This work was supported by the Scientific Service Units of IST Austria through resources provided by the Imaging & Optics, Miba Machine Shop, and Preclinical facilities. G.C. received funding from the European Commission (IST plus postdoctoral fellowship) and S.H. was funded by ISTA institutional funds and the Austrian Science Fund Special Research Programmes (FWF SFB-F78 Neuro Stem Modulation).","ddc":["570"],"OA_type":"gold","publication":"STAR Protocols","volume":5,"citation":{"short":"G.T. Cheung, F. Pauler, P. Koppensteiner, S. Hippenmeyer, STAR Protocols 5 (2024).","ista":"Cheung GT, Pauler F, Koppensteiner P, Hippenmeyer S. 2024. Protocol for mapping cell lineage and cell-type identity of clonally-related cells in situ using MADM-CloneSeq. STAR Protocols. 5(3), 103168.","mla":"Cheung, Giselle T., et al. “Protocol for Mapping Cell Lineage and Cell-Type Identity of Clonally-Related Cells in Situ Using MADM-CloneSeq.” <i>STAR Protocols</i>, vol. 5, no. 3, 103168, Elsevier, 2024, doi:<a href=\"https://doi.org/10.1016/j.xpro.2024.103168\">10.1016/j.xpro.2024.103168</a>.","apa":"Cheung, G. T., Pauler, F., Koppensteiner, P., &#38; Hippenmeyer, S. (2024). Protocol for mapping cell lineage and cell-type identity of clonally-related cells in situ using MADM-CloneSeq. <i>STAR Protocols</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.xpro.2024.103168\">https://doi.org/10.1016/j.xpro.2024.103168</a>","ieee":"G. T. Cheung, F. Pauler, P. Koppensteiner, and S. Hippenmeyer, “Protocol for mapping cell lineage and cell-type identity of clonally-related cells in situ using MADM-CloneSeq,” <i>STAR Protocols</i>, vol. 5, no. 3. Elsevier, 2024.","ama":"Cheung GT, Pauler F, Koppensteiner P, Hippenmeyer S. Protocol for mapping cell lineage and cell-type identity of clonally-related cells in situ using MADM-CloneSeq. <i>STAR Protocols</i>. 2024;5(3). doi:<a href=\"https://doi.org/10.1016/j.xpro.2024.103168\">10.1016/j.xpro.2024.103168</a>","chicago":"Cheung, Giselle T, Florian Pauler, Peter Koppensteiner, and Simon Hippenmeyer. “Protocol for Mapping Cell Lineage and Cell-Type Identity of Clonally-Related Cells in Situ Using MADM-CloneSeq.” <i>STAR Protocols</i>. Elsevier, 2024. <a href=\"https://doi.org/10.1016/j.xpro.2024.103168\">https://doi.org/10.1016/j.xpro.2024.103168</a>."},"type":"journal_article","publisher":"Elsevier","doi":"10.1016/j.xpro.2024.103168","day":"20","article_number":"103168","department":[{"_id":"SiHi"},{"_id":"PreCl"}],"file_date_updated":"2025-01-09T12:16:53Z","date_created":"2024-07-14T22:01:10Z","acknowledged_ssus":[{"_id":"Bio"},{"_id":"M-Shop"},{"_id":"PreCl"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","short":"CC BY-NC-ND (4.0)"},"publication_identifier":{"eissn":["2666-1667"]},"intvolume":"         5","quality_controlled":"1","language":[{"iso":"eng"}],"external_id":{"pmid":["38968076"]},"corr_author":"1","date_updated":"2025-12-30T10:54:12Z","OA_place":"publisher","has_accepted_license":"1"},{"file":[{"success":1,"checksum":"47e94fbe19e86505b429cb7a5b503ce6","file_name":"2023_Cell_Knaus.pdf","date_updated":"2023-05-02T09:26:21Z","content_type":"application/pdf","date_created":"2023-05-02T09:26:21Z","creator":"dernst","access_level":"open_access","file_id":"12889","file_size":15712841,"relation":"main_file"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","isi":1,"oa":1,"project":[{"grant_number":"W1232","_id":"2548AE96-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Molecular Drug Targets"},{"call_identifier":"H2020","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425"},{"call_identifier":"H2020","name":"Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo and in vitro Models","_id":"25444568-B435-11E9-9278-68D0E5697425","grant_number":"715508"}],"publication_status":"published","article_type":"original","author":[{"first_name":"Lisa","id":"3B2ABCF4-F248-11E8-B48F-1D18A9856A87","full_name":"Knaus, Lisa","last_name":"Knaus"},{"last_name":"Basilico","orcid":"0000-0003-1843-3173","first_name":"Bernadette","full_name":"Basilico, Bernadette","id":"36035796-5ACA-11E9-A75E-7AF2E5697425"},{"full_name":"Malzl, Daniel","first_name":"Daniel","last_name":"Malzl"},{"full_name":"Gerykova Bujalkova, Maria","first_name":"Maria","last_name":"Gerykova Bujalkova"},{"last_name":"Smogavec","first_name":"Mateja","full_name":"Smogavec, Mateja"},{"full_name":"Schwarz, Lena A.","first_name":"Lena A.","last_name":"Schwarz"},{"last_name":"Gorkiewicz","id":"f141a35d-15a9-11ec-9fb2-fef6becc7b6f","full_name":"Gorkiewicz, Sarah","first_name":"Sarah"},{"id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","full_name":"Amberg, Nicole","first_name":"Nicole","last_name":"Amberg","orcid":"0000-0002-3183-8207"},{"last_name":"Pauler","orcid":"0000-0002-7462-0048","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","first_name":"Florian"},{"last_name":"Knittl-Frank","full_name":"Knittl-Frank, Christian","first_name":"Christian"},{"last_name":"Tassinari","id":"7af593f1-d44a-11ed-bf94-a3646a6bb35e","full_name":"Tassinari, Marianna","first_name":"Marianna"},{"last_name":"Maulide","full_name":"Maulide, Nuno","first_name":"Nuno"},{"last_name":"Rülicke","first_name":"Thomas","full_name":"Rülicke, Thomas"},{"full_name":"Menche, Jörg","first_name":"Jörg","last_name":"Menche"},{"orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"},{"last_name":"Novarino","orcid":"0000-0002-7673-7178","first_name":"Gaia","full_name":"Novarino, Gaia","id":"3E57A680-F248-11E8-B48F-1D18A9856A87"}],"acknowledgement":"We thank A. Freeman and V. Voronin for technical assistance, S. Deixler, A. Stichelberger, M. Schunn, and the Preclinical Facility for managing our animal colony. We thank L. Andersen and J. Sonntag, who were involved in generating the MADM lines. We thank the ISTA LSF Mass Spectrometry Core Facility for assistance with the proteomic analysis, as well as the ISTA electron microscopy and Imaging and Optics facility for technical support. Metabolomics LC-MS/MS analysis was performed by the Metabolomics Facility at Vienna BioCenter Core Facilities (VBCF). We acknowledge the support of the EMBL Metabolomics Core Facility (MCF) for lipidomics and intracellular metabolomics mass spectrometry data acquisition and analysis. RNA sequencing was performed by the Next Generation Sequencing Facility at VBCF. Schematics were generated using Biorender.com. This work was supported by the Austrian Science Fund (FWF, DK W1232-B24) and by the European Union’s Horizon 2020 research and innovation program (ERC) grant 725780 (LinPro) to S.H. and 715508 (REVERSEAUTISM) to G.N.","ddc":["570"],"abstract":[{"text":"Little is known about the critical metabolic changes that neural cells have to undergo during development and how temporary shifts in this program can influence brain circuitries and behavior. Inspired by the discovery that mutations in SLC7A5, a transporter of metabolically essential large neutral amino acids (LNAAs), lead to autism, we employed metabolomic profiling to study the metabolic states of the cerebral cortex across different developmental stages. We found that the forebrain undergoes significant metabolic remodeling throughout development, with certain groups of metabolites showing stage-specific changes, but what are the consequences of perturbing this metabolic program? By manipulating Slc7a5 expression in neural cells, we found that the metabolism of LNAAs and lipids are interconnected in the cortex. Deletion of Slc7a5 in neurons affects the postnatal metabolic state, leading to a shift in lipid metabolism. Additionally, it causes stage- and cell-type-specific alterations in neuronal activity patterns, resulting in a long-term circuit dysfunction.","lang":"eng"}],"scopus_import":"1","date_published":"2023-04-27T00:00:00Z","status":"public","pmid":1,"month":"04","article_processing_charge":"Yes (via OA deal)","title":"Large neutral amino acid levels tune perinatal neuronal excitability and survival","keyword":["General Biochemistry","Genetics and Molecular Biology"],"year":"2023","_id":"12802","issue":"9","oa_version":"Published Version","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"acknowledged_ssus":[{"_id":"PreCl"},{"_id":"EM-Fac"},{"_id":"Bio"},{"_id":"LifeSc"}],"date_created":"2023-04-05T08:15:40Z","file_date_updated":"2023-05-02T09:26:21Z","department":[{"_id":"SiHi"},{"_id":"GaNo"}],"date_updated":"2026-04-14T08:34:36Z","has_accepted_license":"1","external_id":{"isi":["000991468700001"],"pmid":["36996814"]},"corr_author":"1","intvolume":"       186","quality_controlled":"1","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0092-8674"]},"publication":"Cell","page":"1950-1967.e25","publisher":"Elsevier","doi":"10.1016/j.cell.2023.02.037","day":"27","related_material":{"record":[{"status":"public","id":"19557","relation":"dissertation_contains"},{"relation":"dissertation_contains","id":"13107","status":"public"}],"link":[{"relation":"press_release","description":"News on ISTA Website","url":"https://ista.ac.at/en/news/feed-them-or-lose-them/"}]},"ec_funded":1,"type":"journal_article","citation":{"ista":"Knaus L, Basilico B, Malzl D, Gerykova Bujalkova M, Smogavec M, Schwarz LA, Gorkiewicz S, Amberg N, Pauler F, Knittl-Frank C, Tassinari M, Maulide N, Rülicke T, Menche J, Hippenmeyer S, Novarino G. 2023. Large neutral amino acid levels tune perinatal neuronal excitability and survival. Cell. 186(9), 1950–1967.e25.","apa":"Knaus, L., Basilico, B., Malzl, D., Gerykova Bujalkova, M., Smogavec, M., Schwarz, L. A., … Novarino, G. (2023). Large neutral amino acid levels tune perinatal neuronal excitability and survival. <i>Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cell.2023.02.037\">https://doi.org/10.1016/j.cell.2023.02.037</a>","mla":"Knaus, Lisa, et al. “Large Neutral Amino Acid Levels Tune Perinatal Neuronal Excitability and Survival.” <i>Cell</i>, vol. 186, no. 9, Elsevier, 2023, p. 1950–1967.e25, doi:<a href=\"https://doi.org/10.1016/j.cell.2023.02.037\">10.1016/j.cell.2023.02.037</a>.","ieee":"L. Knaus <i>et al.</i>, “Large neutral amino acid levels tune perinatal neuronal excitability and survival,” <i>Cell</i>, vol. 186, no. 9. Elsevier, p. 1950–1967.e25, 2023.","short":"L. Knaus, B. Basilico, D. Malzl, M. Gerykova Bujalkova, M. Smogavec, L.A. Schwarz, S. Gorkiewicz, N. Amberg, F. Pauler, C. Knittl-Frank, M. Tassinari, N. Maulide, T. Rülicke, J. Menche, S. Hippenmeyer, G. Novarino, Cell 186 (2023) 1950–1967.e25.","chicago":"Knaus, Lisa, Bernadette Basilico, Daniel Malzl, Maria Gerykova Bujalkova, Mateja Smogavec, Lena A. Schwarz, Sarah Gorkiewicz, et al. “Large Neutral Amino Acid Levels Tune Perinatal Neuronal Excitability and Survival.” <i>Cell</i>. Elsevier, 2023. <a href=\"https://doi.org/10.1016/j.cell.2023.02.037\">https://doi.org/10.1016/j.cell.2023.02.037</a>.","ama":"Knaus L, Basilico B, Malzl D, et al. Large neutral amino acid levels tune perinatal neuronal excitability and survival. <i>Cell</i>. 2023;186(9):1950-1967.e25. doi:<a href=\"https://doi.org/10.1016/j.cell.2023.02.037\">10.1016/j.cell.2023.02.037</a>"},"volume":186},{"oa_version":"Published Version","year":"2022","_id":"11449","issue":"6","title":"Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development","article_processing_charge":"No","month":"06","pmid":1,"status":"public","date_published":"2022-06-15T00:00:00Z","scopus_import":"1","abstract":[{"lang":"eng","text":"Mutations are acquired frequently, such that each cell's genome inscribes its history of cell divisions. Common genomic alterations involve loss of heterozygosity (LOH). LOH accumulates throughout the genome, offering large encoding capacity for inferring cell lineage. Using only single-cell RNA sequencing (scRNA-seq) of mouse brain cells, we found that LOH events spanning multiple genes are revealed as tracts of monoallelically expressed, constitutionally heterozygous single-nucleotide variants (SNVs). We simultaneously inferred cell lineage and marked developmental time points based on X chromosome inactivation and the total number of LOH events while identifying cell types from gene expression patterns. Our results are consistent with progenitor cells giving rise to multiple cortical cell types through stereotyped expansion and distinct waves of neurogenesis. This type of retrospective analysis could be incorporated into scRNA-seq pipelines and, compared with experimental approaches for determining lineage in model organisms, is applicable where genetic engineering is prohibited, such as humans."}],"acknowledgement":"D.J.A. thanks Wayne K. Potts, Alan R. Rogers, Kristen Hawkes, Ryk Ward, and Jon Seger for inspiring a young undergraduate to apply evolutionary theory to intraorganism development. Supported by the Paul G. Allen Frontiers Group (University of Washington); NIH R00HG010152 (Dartmouth); and NÖ Forschung und Bildung n[f+b] life science call grant (C13-002) and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program 725780 LinPro to S.H.","author":[{"last_name":"Anderson","first_name":"Donovan J.","full_name":"Anderson, Donovan J."},{"last_name":"Pauler","orcid":"0000-0002-7462-0048","first_name":"Florian","full_name":"Pauler, Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Mckenna","first_name":"Aaron","full_name":"Mckenna, Aaron"},{"last_name":"Shendure","full_name":"Shendure, Jay","first_name":"Jay"},{"orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","first_name":"Simon"},{"last_name":"Horwitz","first_name":"Marshall S.","full_name":"Horwitz, Marshall S."}],"project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780"},{"name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain","_id":"25D92700-B435-11E9-9278-68D0E5697425","grant_number":"LS13-002"}],"article_type":"original","publication_status":"published","oa":1,"isi":1,"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","volume":13,"citation":{"ama":"Anderson DJ, Pauler F, Mckenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development. <i>Cell Systems</i>. 2022;13(6):438-453.e5. doi:<a href=\"https://doi.org/10.1016/j.cels.2022.03.006\">10.1016/j.cels.2022.03.006</a>","chicago":"Anderson, Donovan J., Florian Pauler, Aaron Mckenna, Jay Shendure, Simon Hippenmeyer, and Marshall S. Horwitz. “Simultaneous Brain Cell Type and Lineage Determined by ScRNA-Seq Reveals Stereotyped Cortical Development.” <i>Cell Systems</i>. Elsevier, 2022. <a href=\"https://doi.org/10.1016/j.cels.2022.03.006\">https://doi.org/10.1016/j.cels.2022.03.006</a>.","short":"D.J. Anderson, F. Pauler, A. Mckenna, J. Shendure, S. Hippenmeyer, M.S. Horwitz, Cell Systems 13 (2022) 438–453.e5.","ista":"Anderson DJ, Pauler F, Mckenna A, Shendure J, Hippenmeyer S, Horwitz MS. 2022. Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development. Cell Systems. 13(6), 438–453.e5.","apa":"Anderson, D. J., Pauler, F., Mckenna, A., Shendure, J., Hippenmeyer, S., &#38; Horwitz, M. S. (2022). Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development. <i>Cell Systems</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cels.2022.03.006\">https://doi.org/10.1016/j.cels.2022.03.006</a>","mla":"Anderson, Donovan J., et al. “Simultaneous Brain Cell Type and Lineage Determined by ScRNA-Seq Reveals Stereotyped Cortical Development.” <i>Cell Systems</i>, vol. 13, no. 6, Elsevier, 2022, p. 438–453.e5, doi:<a href=\"https://doi.org/10.1016/j.cels.2022.03.006\">10.1016/j.cels.2022.03.006</a>.","ieee":"D. J. Anderson, F. Pauler, A. Mckenna, J. Shendure, S. Hippenmeyer, and M. S. Horwitz, “Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development,” <i>Cell Systems</i>, vol. 13, no. 6. Elsevier, p. 438–453.e5, 2022."},"type":"journal_article","ec_funded":1,"page":"438-453.e5","publisher":"Elsevier","doi":"10.1016/j.cels.2022.03.006","day":"15","publication":"Cell Systems","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.cels.2022.03.006"}],"publication_identifier":{"issn":["2405-4712"],"eissn":["2405-4720"]},"intvolume":"        13","quality_controlled":"1","language":[{"iso":"eng"}],"external_id":{"pmid":["35452605"],"isi":["000814124400002"]},"date_updated":"2025-04-14T07:43:05Z","department":[{"_id":"SiHi"}],"date_created":"2022-06-19T22:01:57Z"},{"ddc":["570"],"acknowledgement":"We thank A. Heger (IST Austria Preclinical Facility), A. Sommer and C. Czepe (VBCF GmbH, NGS  Unit)  and  S.  Gharagozlou  for  technical  support.  This  research  was  supported  by  the  Scientific  Service  Units  (SSU)  of  IST  Austria  through  resources  provided  by  the  Imaging  &  Optics Facility (IOF), Lab Support Facility (LSF), and Preclinical Facility (PCF). N.A. received funding   from   the   FWF   Firnberg-Programm   (T   1031).   The   work   was   supported   by   IST   institutional  funds  and  by  the  European  Research  Council  (ERC)  under  the  European  Union’s  Horizon 2020 research and innovation program (grant agreement 725780 LinPro) to S.H.","date_published":"2022-11-01T00:00:00Z","abstract":[{"text":"The generation of a correctly-sized cerebral cortex with all-embracing neuronal and glial cell-type diversity critically depends on faithful radial glial progenitor (RGP) cell proliferation/differentiation programs. Temporal RGP lineage progression is regulated by Polycomb Repressive Complex 2 (PRC2) and loss of PRC2 activity results in severe neurogenesis defects and microcephaly. How PRC2-dependent gene expression instructs RGP lineage progression is unknown. Here we utilize Mosaic Analysis with Double Markers (MADM)-based single cell technology and demonstrate that PRC2 is not cell-autonomously required in neurogenic RGPs but rather acts at the global tissue-wide level. Conversely, cortical astrocyte production and maturation is cell-autonomously controlled by PRC2-dependent transcriptional regulation. We thus reveal highly distinct and sequential PRC2 functions in RGP lineage progression that are dependent on complex interplays between intrinsic and tissue-wide properties. In a broader context our results imply a critical role for the genetic and cellular niche environment in neural stem cell behavior.","lang":"eng"}],"scopus_import":"1","status":"public","isi":1,"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","file":[{"creator":"patrickd","date_created":"2023-03-21T14:18:10Z","access_level":"open_access","content_type":"application/pdf","relation":"main_file","file_size":2973998,"file_id":"12742","checksum":"0117023e188542082ca6693cf39e7f03","success":1,"file_name":"sciadv.abq1263.pdf","date_updated":"2023-03-21T14:18:10Z"}],"oa":1,"publication_status":"published","article_type":"original","project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780"},{"grant_number":"T01031","_id":"268F8446-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Role of Eed in neural stem cell lineage progression"}],"author":[{"last_name":"Amberg","orcid":"0000-0002-3183-8207","first_name":"Nicole","full_name":"Amberg, Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0002-7462-0048","last_name":"Pauler","full_name":"Pauler, Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","first_name":"Florian"},{"full_name":"Streicher, Carmen","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","first_name":"Carmen","last_name":"Streicher"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","first_name":"Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"}],"title":"Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression","issue":"44","_id":"11336","year":"2022","oa_version":"Published Version","pmid":1,"month":"11","article_processing_charge":"No","has_accepted_license":"1","date_updated":"2025-09-09T14:30:38Z","corr_author":"1","external_id":{"pmid":["36322669"],"isi":["000918406800019"]},"language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"         8","publication_identifier":{"issn":["2375-2548"]},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"acknowledged_ssus":[{"_id":"PreCl"},{"_id":"Bio"},{"_id":"LifeSc"}],"date_created":"2022-04-26T15:04:50Z","file_date_updated":"2023-03-21T14:18:10Z","department":[{"_id":"SiHi"}],"article_number":"abq1263","day":"01","publisher":"American Association for the Advancement of Science","doi":"10.1126/sciadv.abq1263","ec_funded":1,"type":"journal_article","related_material":{"link":[{"url":"https://ista.ac.at/en/news/whole-tissue-shapes-brain-development/","relation":"press_release","description":"News on ISTA website"}]},"citation":{"short":"N. Amberg, F. Pauler, C. Streicher, S. Hippenmeyer, Science Advances 8 (2022).","ista":"Amberg N, Pauler F, Streicher C, Hippenmeyer S. 2022. Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression. Science Advances. 8(44), abq1263.","apa":"Amberg, N., Pauler, F., Streicher, C., &#38; Hippenmeyer, S. (2022). Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression. <i>Science Advances</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/sciadv.abq1263\">https://doi.org/10.1126/sciadv.abq1263</a>","mla":"Amberg, Nicole, et al. “Tissue-Wide Genetic and Cellular Landscape Shapes the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression.” <i>Science Advances</i>, vol. 8, no. 44, abq1263, American Association for the Advancement of Science, 2022, doi:<a href=\"https://doi.org/10.1126/sciadv.abq1263\">10.1126/sciadv.abq1263</a>.","ieee":"N. Amberg, F. Pauler, C. Streicher, and S. Hippenmeyer, “Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression,” <i>Science Advances</i>, vol. 8, no. 44. American Association for the Advancement of Science, 2022.","ama":"Amberg N, Pauler F, Streicher C, Hippenmeyer S. Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression. <i>Science Advances</i>. 2022;8(44). doi:<a href=\"https://doi.org/10.1126/sciadv.abq1263\">10.1126/sciadv.abq1263</a>","chicago":"Amberg, Nicole, Florian Pauler, Carmen Streicher, and Simon Hippenmeyer. “Tissue-Wide Genetic and Cellular Landscape Shapes the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression.” <i>Science Advances</i>. American Association for the Advancement of Science, 2022. <a href=\"https://doi.org/10.1126/sciadv.abq1263\">https://doi.org/10.1126/sciadv.abq1263</a>."},"volume":8,"publication":"Science Advances"},{"volume":1,"citation":{"chicago":"Hansen, Andi H, Florian Pauler, Michael Riedl, Carmen Streicher, Anna-Magdalena Heger, Susanne Laukoter, Christoph M Sommer, et al. “Tissue-Wide Effects Override Cell-Intrinsic Gene Function in Radial Neuron Migration.” <i>Oxford Open Neuroscience</i>. Oxford University Press, 2022. <a href=\"https://doi.org/10.1093/oons/kvac009\">https://doi.org/10.1093/oons/kvac009</a>.","ama":"Hansen AH, Pauler F, Riedl M, et al. Tissue-wide effects override cell-intrinsic gene function in radial neuron migration. <i>Oxford Open Neuroscience</i>. 2022;1(1). doi:<a href=\"https://doi.org/10.1093/oons/kvac009\">10.1093/oons/kvac009</a>","ieee":"A. H. Hansen <i>et al.</i>, “Tissue-wide effects override cell-intrinsic gene function in radial neuron migration,” <i>Oxford Open Neuroscience</i>, vol. 1, no. 1. Oxford University Press, 2022.","mla":"Hansen, Andi H., et al. “Tissue-Wide Effects Override Cell-Intrinsic Gene Function in Radial Neuron Migration.” <i>Oxford Open Neuroscience</i>, vol. 1, no. 1, kvac009, Oxford University Press, 2022, doi:<a href=\"https://doi.org/10.1093/oons/kvac009\">10.1093/oons/kvac009</a>.","apa":"Hansen, A. H., Pauler, F., Riedl, M., Streicher, C., Heger, A.-M., Laukoter, S., … Hippenmeyer, S. (2022). Tissue-wide effects override cell-intrinsic gene function in radial neuron migration. <i>Oxford Open Neuroscience</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/oons/kvac009\">https://doi.org/10.1093/oons/kvac009</a>","ista":"Hansen AH, Pauler F, Riedl M, Streicher C, Heger A-M, Laukoter S, Sommer CM, Nicolas A, Hof B, Tsai LH, Rülicke T, Hippenmeyer S. 2022. Tissue-wide effects override cell-intrinsic gene function in radial neuron migration. Oxford Open Neuroscience. 1(1), kvac009.","short":"A.H. Hansen, F. Pauler, M. Riedl, C. Streicher, A.-M. Heger, S. Laukoter, C.M. Sommer, A. Nicolas, B. Hof, L.H. Tsai, T. Rülicke, S. Hippenmeyer, Oxford Open Neuroscience 1 (2022)."},"ec_funded":1,"type":"journal_article","related_material":{"record":[{"status":"public","id":"12726","relation":"dissertation_contains"},{"id":"14530","relation":"dissertation_contains","status":"public"}]},"day":"07","doi":"10.1093/oons/kvac009","publisher":"Oxford University Press","publication":"Oxford Open Neuroscience","publication_identifier":{"eissn":["2753-149X"]},"quality_controlled":"1","language":[{"iso":"eng"}],"intvolume":"         1","corr_author":"1","external_id":{"pmid":["38596707"]},"has_accepted_license":"1","date_updated":"2026-04-07T13:29:13Z","department":[{"_id":"SiHi"},{"_id":"BjHo"},{"_id":"LifeSc"},{"_id":"EM-Fac"}],"article_number":"kvac009","date_created":"2022-02-25T07:52:11Z","file_date_updated":"2023-08-16T08:00:30Z","acknowledged_ssus":[{"_id":"LifeSc"},{"_id":"PreCl"},{"_id":"Bio"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"oa_version":"Published Version","issue":"1","_id":"10791","year":"2022","title":"Tissue-wide effects override cell-intrinsic gene function in radial neuron migration","article_processing_charge":"No","month":"07","pmid":1,"status":"public","abstract":[{"text":"The mammalian neocortex is composed of diverse neuronal and glial cell classes that broadly arrange in six distinct laminae. Cortical layers emerge during development and defects in the developmental programs that orchestrate cortical lamination are associated with neurodevelopmental diseases. The developmental principle of cortical layer formation depends on concerted radial projection neuron migration, from their birthplace to their final target position. Radial migration occurs in defined sequential steps, regulated by a large array of signaling pathways. However, based on genetic loss-of-function experiments, most studies have thus far focused on the role of cell-autonomous gene function. Yet, cortical neuron migration in situ is a complex process and migrating neurons traverse along diverse cellular compartments and environments. The role of tissue-wide properties and genetic state in radial neuron migration is however not clear. Here we utilized mosaic analysis with double markers (MADM) technology to either sparsely or globally delete gene function, followed by quantitative single-cell phenotyping. The MADM-based gene ablation paradigms in combination with computational modeling demonstrated that global tissue-wide effects predominate cell-autonomous gene function albeit in a gene-specific manner. Our results thus suggest that the genetic landscape in a tissue critically affects the overall migration phenotype of individual cortical projection neurons. In a broader context, our findings imply that global tissue-wide effects represent an essential component of the underlying etiology associated with focal malformations of cortical development in particular, and neurological diseases in general.","lang":"eng"}],"date_published":"2022-07-07T00:00:00Z","ddc":["570"],"acknowledgement":"A.H.H. was a recipient of a DOC Fellowship (24812) of the Austrian Academy of Sciences. This work also received support from IST Austria institutional funds; the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007–2013) under REA grant agreement No 618444 to S.H.\r\nAPC funding was obtained by IST Austria institutional funds.\r\nWe thank A. Sommer and C. Czepe (VBCF GmbH, NGS Unit), L. Andersen, J. Sonntag and J. Renno for technical support and/or initial experiments; M. Sixt, J. Nimpf and all members of the Hippenmeyer lab for discussion. This research was supported by the Scientific Service Units of IST Austria through resources provided by the Imaging and Optics Facility, Lab Support Facility and Preclinical Facility.","author":[{"first_name":"Andi H","full_name":"Hansen, Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87","last_name":"Hansen"},{"id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","first_name":"Florian","last_name":"Pauler","orcid":"0000-0002-7462-0048"},{"full_name":"Riedl, Michael","id":"3BE60946-F248-11E8-B48F-1D18A9856A87","first_name":"Michael","last_name":"Riedl","orcid":"0000-0003-4844-6311"},{"last_name":"Streicher","first_name":"Carmen","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","full_name":"Streicher, Carmen"},{"last_name":"Heger","full_name":"Heger, Anna-Magdalena","id":"4B76FFD2-F248-11E8-B48F-1D18A9856A87","first_name":"Anna-Magdalena"},{"orcid":"0000-0002-7903-3010","last_name":"Laukoter","full_name":"Laukoter, Susanne","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","first_name":"Susanne"},{"first_name":"Christoph M","full_name":"Sommer, Christoph M","id":"4DF26D8C-F248-11E8-B48F-1D18A9856A87","last_name":"Sommer","orcid":"0000-0003-1216-9105"},{"last_name":"Nicolas","id":"2A103192-F248-11E8-B48F-1D18A9856A87","full_name":"Nicolas, Armel","first_name":"Armel"},{"last_name":"Hof","orcid":"0000-0003-2057-2754","id":"3A374330-F248-11E8-B48F-1D18A9856A87","full_name":"Hof, Björn","first_name":"Björn"},{"last_name":"Tsai","first_name":"Li Huei","full_name":"Tsai, Li Huei"},{"first_name":"Thomas","full_name":"Rülicke, Thomas","last_name":"Rülicke"},{"last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","first_name":"Simon"}],"publication_status":"published","article_type":"original","project":[{"grant_number":"618444","_id":"25D61E48-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Molecular Mechanisms of Cerebral Cortex Development"},{"grant_number":"24812","_id":"2625A13E-B435-11E9-9278-68D0E5697425","name":"Molecular mechanisms of radial neuronal migration"}],"oa":1,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file":[{"date_created":"2023-08-16T08:00:30Z","creator":"dernst","access_level":"open_access","content_type":"application/pdf","file_size":4846551,"relation":"main_file","file_id":"14061","checksum":"822e76e056c07099d1fb27d1ece5941b","success":1,"file_name":"2023_OxfordOpenNeuroscience_Hansen.pdf","date_updated":"2023-08-16T08:00:30Z"}]},{"oa":1,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"SiHi"}],"author":[{"first_name":"Donovan J.","full_name":"Anderson, Donovan J.","last_name":"Anderson"},{"first_name":"Florian","full_name":"Pauler, Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","last_name":"Pauler","orcid":"0000-0002-7462-0048"},{"full_name":"McKenna, Aaron","first_name":"Aaron","last_name":"McKenna"},{"last_name":"Shendure","full_name":"Shendure, Jay","first_name":"Jay"},{"full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061"},{"last_name":"Horwitz","first_name":"Marshall S.","full_name":"Horwitz, Marshall S."}],"publication_status":"submitted","date_created":"2021-02-04T07:23:23Z","project":[{"_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780","call_identifier":"H2020","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"}],"acknowledgement":"We thank Bill Bolosky, Microsoft Research, for earlier work showing proof of concept in TCGA\r\nbulk RNA-seq data. Supported by the Paul G. Allen Frontiers Group (University of Washington);\r\nNIH R00HG010152 (Dartmouth); and NÖ Forschung und Bildung n[f+b] life science call grant\r\n(C13-002) to SH, and the European Research Council (ERC) under the European Union’s\r\nHorizon 2020 research and innovation program 725780 LinPro to SH.","date_updated":"2025-04-14T07:43:04Z","status":"public","language":[{"iso":"eng"}],"abstract":[{"text":"Acquired mutations are sufficiently frequent such that the genome of a single cell offers a record of its history of cell divisions. Among more common somatic genomic alterations are loss of heterozygosity (LOH). Large LOH events are potentially detectable in single cell RNA sequencing (scRNA-seq) datasets as tracts of monoallelic expression for constitutionally heterozygous single nucleotide variants (SNVs) located among contiguous genes. We identified runs of monoallelic expression, consistent with LOH, uniquely distributed throughout the genome in single cell brain cortex transcriptomes of F1 hybrids involving different inbred mouse strains. We then phylogenetically reconstructed single cell lineages and simultaneously identified cell types by corresponding gene expression patterns. Our results are consistent with progenitor cells giving rise to multiple cortical cell types through stereotyped expansion and distinct waves of neurogenesis. Compared to engineered recording systems, LOH events accumulate throughout the genome and across the lifetime of an organism, affording tremendous capacity for encoding lineage information and increasing resolution for later cell divisions. This approach can conceivably be computationally incorporated into scRNA-seq analysis and may be useful for organisms where genetic engineering is prohibitive, such as humans.","lang":"eng"}],"date_published":"2021-01-01T00:00:00Z","month":"01","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/2020.12.31.425016"}],"article_processing_charge":"No","publication":"bioRxiv","ec_funded":1,"type":"preprint","title":"Simultaneous identification of brain cell type and lineage via single cell RNA sequencing","doi":"10.1101/2020.12.31.425016","publisher":"Cold Spring Harbor Laboratory","day":"01","oa_version":"Preprint","_id":"9082","citation":{"ama":"Anderson DJ, Pauler F, McKenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous identification of brain cell type and lineage via single cell RNA sequencing. <i>bioRxiv</i>. doi:<a href=\"https://doi.org/10.1101/2020.12.31.425016\">10.1101/2020.12.31.425016</a>","chicago":"Anderson, Donovan J., Florian Pauler, Aaron McKenna, Jay Shendure, Simon Hippenmeyer, and Marshall S. Horwitz. “Simultaneous Identification of Brain Cell Type and Lineage via Single Cell RNA Sequencing.” <i>BioRxiv</i>. Cold Spring Harbor Laboratory, n.d. <a href=\"https://doi.org/10.1101/2020.12.31.425016\">https://doi.org/10.1101/2020.12.31.425016</a>.","short":"D.J. Anderson, F. Pauler, A. McKenna, J. Shendure, S. Hippenmeyer, M.S. Horwitz, BioRxiv (n.d.).","ieee":"D. J. Anderson, F. Pauler, A. McKenna, J. Shendure, S. Hippenmeyer, and M. S. Horwitz, “Simultaneous identification of brain cell type and lineage via single cell RNA sequencing,” <i>bioRxiv</i>. Cold Spring Harbor Laboratory.","mla":"Anderson, Donovan J., et al. “Simultaneous Identification of Brain Cell Type and Lineage via Single Cell RNA Sequencing.” <i>BioRxiv</i>, Cold Spring Harbor Laboratory, doi:<a href=\"https://doi.org/10.1101/2020.12.31.425016\">10.1101/2020.12.31.425016</a>.","apa":"Anderson, D. J., Pauler, F., McKenna, A., Shendure, J., Hippenmeyer, S., &#38; Horwitz, M. S. (n.d.). Simultaneous identification of brain cell type and lineage via single cell RNA sequencing. <i>bioRxiv</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/2020.12.31.425016\">https://doi.org/10.1101/2020.12.31.425016</a>","ista":"Anderson DJ, Pauler F, McKenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous identification of brain cell type and lineage via single cell RNA sequencing. bioRxiv, <a href=\"https://doi.org/10.1101/2020.12.31.425016\">10.1101/2020.12.31.425016</a>."},"year":"2021"},{"publication_status":"published","article_type":"original","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"},{"grant_number":"LS13-002","_id":"25D92700-B435-11E9-9278-68D0E5697425","name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain"}],"author":[{"orcid":"0000-0002-7462-0048","last_name":"Pauler","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","first_name":"Florian"},{"last_name":"Hudson","full_name":"Hudson, Quanah","first_name":"Quanah"},{"id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","full_name":"Laukoter, Susanne","first_name":"Susanne","last_name":"Laukoter","orcid":"0000-0002-7903-3010"},{"full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","isi":1,"file":[{"file_name":"2021_NCI_Pauler.pdf","date_updated":"2021-08-11T12:30:38Z","success":1,"checksum":"c6d7a40089cd29e289f9b22e75768304","file_id":"9883","relation":"main_file","file_size":7083499,"content_type":"application/pdf","date_created":"2021-08-11T12:30:38Z","creator":"kschuh","access_level":"open_access"}],"oa":1,"date_published":"2021-05-01T00:00:00Z","scopus_import":"1","abstract":[{"text":"Genomic imprinting is an epigenetic mechanism that results in parental allele-specific expression of ~1% of all genes in mouse and human. Imprinted genes are key developmental regulators and play pivotal roles in many biological processes such as nutrient transfer from the mother to offspring and neuronal development. Imprinted genes are also involved in human disease, including neurodevelopmental disorders, and often occur in clusters that are regulated by a common imprint control region (ICR). In extra-embryonic tissues ICRs can act over large distances, with the largest surrounding Igf2r spanning over 10 million base-pairs. Besides classical imprinted expression that shows near exclusive maternal or paternal expression, widespread biased imprinted expression has been identified mainly in brain. In this review we discuss recent developments mapping cell type specific imprinted expression in extra-embryonic tissues and neocortex in the mouse. We highlight the advantages of using an inducible uniparental chromosome disomy (UPD) system to generate cells carrying either two maternal or two paternal copies of a specific chromosome to analyze the functional consequences of genomic imprinting. Mosaic Analysis with Double Markers (MADM) allows fluorescent labeling and concomitant induction of UPD sparsely in specific cell types, and thus to over-express or suppress all imprinted genes on that chromosome. To illustrate the utility of this technique, we explain how MADM-induced UPD revealed new insights about the function of the well-studied Cdkn1c imprinted gene, and how MADM-induced UPDs led to identification of highly cell type specific phenotypes related to perturbed imprinted expression in the mouse neocortex. Finally, we give an outlook on how MADM could be used to probe cell type specific imprinted expression in other tissues in mouse, particularly in extra-embryonic tissues.","lang":"eng"}],"status":"public","ddc":["570"],"acknowledgement":"We thank Melissa Stouffer for critically reading the manuscript. This work was supported by IST Austria institutional funds; NÖ Forschung und Bildung n[f + b] life science call grant (C13-002) to S.H. and the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program (grant agreement 725780 LinPro) to S.H.","article_processing_charge":"Yes (via OA deal)","pmid":1,"month":"05","issue":"5","_id":"9188","year":"2021","oa_version":"Published Version","keyword":["Cell Biology","Cellular and Molecular Neuroscience"],"title":"Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond","file_date_updated":"2021-08-11T12:30:38Z","date_created":"2021-02-23T12:31:43Z","department":[{"_id":"SiHi"}],"article_number":"104986","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","short":"CC BY-NC-ND (4.0)"},"language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"       145","publication_identifier":{"issn":["0197-0186"]},"has_accepted_license":"1","date_updated":"2025-04-14T07:43:04Z","external_id":{"isi":["000635575000005"],"pmid":["33600873"]},"publication":"Neurochemistry International","citation":{"chicago":"Pauler, Florian, Quanah Hudson, Susanne Laukoter, and Simon Hippenmeyer. “Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell Level in Brain and Beyond.” <i>Neurochemistry International</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.neuint.2021.104986\">https://doi.org/10.1016/j.neuint.2021.104986</a>.","ama":"Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. <i>Neurochemistry International</i>. 2021;145(5). doi:<a href=\"https://doi.org/10.1016/j.neuint.2021.104986\">10.1016/j.neuint.2021.104986</a>","ieee":"F. Pauler, Q. Hudson, S. Laukoter, and S. Hippenmeyer, “Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond,” <i>Neurochemistry International</i>, vol. 145, no. 5. Elsevier, 2021.","ista":"Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. 2021. Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry International. 145(5), 104986.","apa":"Pauler, F., Hudson, Q., Laukoter, S., &#38; Hippenmeyer, S. (2021). Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. <i>Neurochemistry International</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuint.2021.104986\">https://doi.org/10.1016/j.neuint.2021.104986</a>","mla":"Pauler, Florian, et al. “Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell Level in Brain and Beyond.” <i>Neurochemistry International</i>, vol. 145, no. 5, 104986, Elsevier, 2021, doi:<a href=\"https://doi.org/10.1016/j.neuint.2021.104986\">10.1016/j.neuint.2021.104986</a>.","short":"F. Pauler, Q. Hudson, S. Laukoter, S. Hippenmeyer, Neurochemistry International 145 (2021)."},"volume":145,"day":"01","publisher":"Elsevier","doi":"10.1016/j.neuint.2021.104986","ec_funded":1,"type":"journal_article"},{"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"file_date_updated":"2021-08-16T09:29:17Z","date_created":"2021-08-15T22:01:27Z","department":[{"_id":"SiHi"}],"article_number":"8385","has_accepted_license":"1","date_updated":"2025-06-12T06:29:07Z","external_id":{"pmid":["34445100"],"isi":["000689147400001"]},"quality_controlled":"1","language":[{"iso":"eng"}],"intvolume":"        22","publication_identifier":{"issn":["1661-6596"],"eissn":["1422-0067"]},"publication":"International Journal of Molecular Sciences","doi":"10.3390/ijms22168385","publisher":"MDPI","day":"04","type":"journal_article","citation":{"short":"I. Yotova, Q.J. Hudson, F. Pauler, K. Proestling, I. Haslinger, L. Kuessel, A. Perricos, H. Husslein, R. Wenzl, International Journal of Molecular Sciences 22 (2021).","apa":"Yotova, I., Hudson, Q. J., Pauler, F., Proestling, K., Haslinger, I., Kuessel, L., … Wenzl, R. (2021). LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line. <i>International Journal of Molecular Sciences</i>. MDPI. <a href=\"https://doi.org/10.3390/ijms22168385\">https://doi.org/10.3390/ijms22168385</a>","mla":"Yotova, Iveta, et al. “LINC01133 Inhibits Invasion and Promotes Proliferation in an Endometriosis Epithelial Cell Line.” <i>International Journal of Molecular Sciences</i>, vol. 22, no. 16, 8385, MDPI, 2021, doi:<a href=\"https://doi.org/10.3390/ijms22168385\">10.3390/ijms22168385</a>.","ista":"Yotova I, Hudson QJ, Pauler F, Proestling K, Haslinger I, Kuessel L, Perricos A, Husslein H, Wenzl R. 2021. LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line. International Journal of Molecular Sciences. 22(16), 8385.","ieee":"I. Yotova <i>et al.</i>, “LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line,” <i>International Journal of Molecular Sciences</i>, vol. 22, no. 16. MDPI, 2021.","ama":"Yotova I, Hudson QJ, Pauler F, et al. LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line. <i>International Journal of Molecular Sciences</i>. 2021;22(16). doi:<a href=\"https://doi.org/10.3390/ijms22168385\">10.3390/ijms22168385</a>","chicago":"Yotova, Iveta, Quanah J. Hudson, Florian Pauler, Katharina Proestling, Isabella Haslinger, Lorenz Kuessel, Alexandra Perricos, Heinrich Husslein, and René Wenzl. “LINC01133 Inhibits Invasion and Promotes Proliferation in an Endometriosis Epithelial Cell Line.” <i>International Journal of Molecular Sciences</i>. MDPI, 2021. <a href=\"https://doi.org/10.3390/ijms22168385\">https://doi.org/10.3390/ijms22168385</a>."},"volume":22,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","isi":1,"file":[{"file_id":"9922","file_size":2646018,"relation":"main_file","content_type":"application/pdf","access_level":"open_access","creator":"asandaue","date_created":"2021-08-16T09:29:17Z","date_updated":"2021-08-16T09:29:17Z","file_name":"2021_InternationalJournalOfMolecularSciences_Yotova.pdf","success":1,"checksum":"be7f0042607ca60549cb27513c19c6af"}],"oa":1,"article_type":"original","publication_status":"published","author":[{"last_name":"Yotova","first_name":"Iveta","full_name":"Yotova, Iveta"},{"first_name":"Quanah J.","full_name":"Hudson, Quanah J.","last_name":"Hudson"},{"orcid":"0000-0002-7462-0048","last_name":"Pauler","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","first_name":"Florian"},{"full_name":"Proestling, Katharina","first_name":"Katharina","last_name":"Proestling"},{"last_name":"Haslinger","full_name":"Haslinger, Isabella","first_name":"Isabella"},{"last_name":"Kuessel","full_name":"Kuessel, Lorenz","first_name":"Lorenz"},{"full_name":"Perricos, Alexandra","first_name":"Alexandra","last_name":"Perricos"},{"first_name":"Heinrich","full_name":"Husslein, Heinrich","last_name":"Husslein"},{"last_name":"Wenzl","first_name":"René","full_name":"Wenzl, René"}],"ddc":["570"],"acknowledgement":"Open access funding provided by Medical University of Vienna. The authors would like to thank all the participants and health professionals involved in the present study. We want to thank our technical assistants Barbara Widmar and Matthias Witzmann-Stern for their diligent work and constant assistance. We would like to thank Simon Hippenmeyer for access to\r\nbioinformatic infrastructure and resources.","abstract":[{"text":"Endometriosis is a common gynecological disorder characterized by ectopic growth of endometrium outside the uterus and is associated with chronic pain and infertility. We investigated the role of the long intergenic noncoding RNA 01133 (LINC01133) in endometriosis, an lncRNA that has been implicated in several types of cancer. We found that LINC01133 is upregulated in ectopic endometriotic lesions. As expression appeared higher in the epithelial endometrial layer, we performed a siRNA knockdown of LINC01133 in an endometriosis epithelial cell line. Phenotypic assays indicated that LINC01133 may promote proliferation and suppress cellular migration, and affect the cytoskeleton and morphology of the cells. Gene ontology analysis of differentially expressed genes indicated that cell proliferation and migration pathways were affected in line with the observed phenotype. We validated upregulation of p21 and downregulation of Cyclin A at the protein level, which together with the quantification of the DNA content using fluorescence-activated cell sorting (FACS) analysis indicated that the observed effects on cellular proliferation may be due to changes in cell cycle. Further, we found testis-specific protein kinase 1 (TESK1) kinase upregulation corresponding with phosphorylation and inactivation of actin severing protein Cofilin, which could explain changes in the cytoskeleton and cellular migration. These results indicate that endometriosis is associated with LINC01133 upregulation, which may affect pathogenesis via the cellular proliferation and migration pathways.","lang":"eng"}],"date_published":"2021-08-04T00:00:00Z","scopus_import":"1","status":"public","pmid":1,"month":"08","article_processing_charge":"Yes","title":"LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line","issue":"16","_id":"9906","year":"2021","oa_version":"Published Version"},{"date_published":"2021-07-12T00:00:00Z","scopus_import":"1","abstract":[{"lang":"eng","text":"In mammalian genomes, differentially methylated regions (DMRs) and histone marks including trimethylation of histone 3 lysine 27 (H3K27me3) at imprinted genes are asymmetrically inherited to control parentally-biased gene expression. However, neither parent-of-origin-specific transcription nor imprints have been comprehensively mapped at the blastocyst stage of preimplantation development. Here, we address this by integrating transcriptomic and epigenomic approaches in mouse preimplantation embryos. We find that seventy-one genes exhibit previously unreported parent-of-origin-specific expression in blastocysts (nBiX: novel blastocyst-imprinted expressed). Uniparental expression of nBiX genes disappears soon after implantation. Micro-whole-genome bisulfite sequencing (µWGBS) of individual uniparental blastocysts detects 859 DMRs. We further find that 16% of nBiX genes are associated with a DMR, whereas most are associated with parentally-biased H3K27me3, suggesting a role for Polycomb-mediated imprinting in blastocysts. nBiX genes are clustered: five clusters contained at least one published imprinted gene, and five clusters exclusively contained nBiX genes. These data suggest that early development undergoes a complex program of stage-specific imprinting involving different tiers of regulation."}],"status":"public","ddc":["570"],"acknowledgement":"The authors thank Robert Feil and Anton Wutz for helpful discussions and comments, Samuel Collombet and Peter Fraser for sharing embryo TAD coordinates, and Andy Riddel at the Cambridge Stem Cell Institute and Thomas Sauer at the Max Perutz Laboratories FACS facility for flow-sorting. We thank the team of the Biomedical Sequencing Facility at the CeMM and the Vienna Biocenter Core Facilities (VBCF) for support with next-generation sequencing. We are grateful to animal care teams at the University of Bath and MRC Harwell. A.C.F.P. acknowledges support from the UK Medical Research Council (MR/N000080/1 and MR/N020294/1) and Biotechnology and Biological Sciences Research Council (BB/P009506/1). L.S. is part of the FWF doctoral programme SMICH and supported by an Austrian Academy of Sciences DOC Fellowship. M.L. is funded by a Vienna Research Group for Young Investigators grant (VRG14-006) by the Vienna Science and Technology Fund (WWTF) and by the Austrian Science Fund FWF (I3786 and P31334).","publication_status":"published","article_type":"original","author":[{"last_name":"Santini","full_name":"Santini, Laura","first_name":"Laura"},{"first_name":"Florian","full_name":"Halbritter, Florian","last_name":"Halbritter"},{"full_name":"Titz-Teixeira, Fabian","first_name":"Fabian","last_name":"Titz-Teixeira"},{"last_name":"Suzuki","first_name":"Toru","full_name":"Suzuki, Toru"},{"last_name":"Asami","full_name":"Asami, Maki","first_name":"Maki"},{"full_name":"Ma, Xiaoyan","first_name":"Xiaoyan","last_name":"Ma"},{"first_name":"Julia","full_name":"Ramesmayer, Julia","last_name":"Ramesmayer"},{"first_name":"Andreas","full_name":"Lackner, Andreas","last_name":"Lackner"},{"last_name":"Warr","first_name":"Nick","full_name":"Warr, Nick"},{"last_name":"Pauler","orcid":"0000-0002-7462-0048","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","first_name":"Florian"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","first_name":"Simon","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061"},{"full_name":"Laue, Ernest","first_name":"Ernest","last_name":"Laue"},{"full_name":"Farlik, Matthias","first_name":"Matthias","last_name":"Farlik"},{"last_name":"Bock","first_name":"Christoph","full_name":"Bock, Christoph"},{"last_name":"Beyer","full_name":"Beyer, Andreas","first_name":"Andreas"},{"full_name":"Perry, Anthony C.F.","first_name":"Anthony C.F.","last_name":"Perry"},{"last_name":"Leeb","full_name":"Leeb, Martin","first_name":"Martin"}],"isi":1,"user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","file":[{"file_name":"2021_NatureCommunications_Santini.pdf","date_updated":"2021-06-28T08:04:22Z","success":1,"checksum":"75dd89d09945185b2d14b2434a0bcb50","file_id":"9608","relation":"main_file","file_size":2156554,"content_type":"application/pdf","date_created":"2021-06-28T08:04:22Z","creator":"asandaue","access_level":"open_access"}],"oa":1,"_id":"9601","issue":"1","year":"2021","oa_version":"Published Version","title":"Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3","article_processing_charge":"No","month":"07","language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"        12","publication_identifier":{"eissn":["2041-1723"]},"has_accepted_license":"1","date_updated":"2026-04-02T13:55:23Z","external_id":{"isi":["000667248600005"]},"date_created":"2021-06-27T22:01:46Z","file_date_updated":"2021-06-28T08:04:22Z","department":[{"_id":"SiHi"}],"article_number":"3804","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"citation":{"ama":"Santini L, Halbritter F, Titz-Teixeira F, et al. Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3. <i>Nature Communications</i>. 2021;12(1). doi:<a href=\"https://doi.org/10.1038/s41467-021-23510-4\">10.1038/s41467-021-23510-4</a>","chicago":"Santini, Laura, Florian Halbritter, Fabian Titz-Teixeira, Toru Suzuki, Maki Asami, Xiaoyan Ma, Julia Ramesmayer, et al. “Genomic Imprinting in Mouse Blastocysts Is Predominantly Associated with H3K27me3.” <i>Nature Communications</i>. Springer Nature, 2021. <a href=\"https://doi.org/10.1038/s41467-021-23510-4\">https://doi.org/10.1038/s41467-021-23510-4</a>.","short":"L. Santini, F. Halbritter, F. Titz-Teixeira, T. Suzuki, M. Asami, X. Ma, J. Ramesmayer, A. Lackner, N. Warr, F. Pauler, S. Hippenmeyer, E. Laue, M. Farlik, C. Bock, A. Beyer, A.C.F. Perry, M. Leeb, Nature Communications 12 (2021).","ieee":"L. Santini <i>et al.</i>, “Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3,” <i>Nature Communications</i>, vol. 12, no. 1. Springer Nature, 2021.","ista":"Santini L, Halbritter F, Titz-Teixeira F, Suzuki T, Asami M, Ma X, Ramesmayer J, Lackner A, Warr N, Pauler F, Hippenmeyer S, Laue E, Farlik M, Bock C, Beyer A, Perry ACF, Leeb M. 2021. Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3. Nature Communications. 12(1), 3804.","mla":"Santini, Laura, et al. “Genomic Imprinting in Mouse Blastocysts Is Predominantly Associated with H3K27me3.” <i>Nature Communications</i>, vol. 12, no. 1, 3804, Springer Nature, 2021, doi:<a href=\"https://doi.org/10.1038/s41467-021-23510-4\">10.1038/s41467-021-23510-4</a>.","apa":"Santini, L., Halbritter, F., Titz-Teixeira, F., Suzuki, T., Asami, M., Ma, X., … Leeb, M. (2021). Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-021-23510-4\">https://doi.org/10.1038/s41467-021-23510-4</a>"},"volume":12,"publisher":"Springer Nature","day":"12","doi":"10.1038/s41467-021-23510-4","type":"journal_article","publication":"Nature Communications"},{"file_date_updated":"2020-07-14T12:48:03Z","date_created":"2020-05-11T08:18:48Z","department":[{"_id":"SiHi"}],"article_number":"48","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"},{"_id":"PreCl"},{"_id":"EM-Fac"}],"language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"         5","publication_identifier":{"issn":["2504-284X"]},"has_accepted_license":"1","date_updated":"2024-10-22T10:46:38Z","corr_author":"1","publication":"Frontiers in Education","citation":{"ieee":"R. J. Beattie, S. Hippenmeyer, and F. Pauler, “SCOPES: Sparking curiosity through Open-Source platforms in education and science,” <i>Frontiers in Education</i>, vol. 5. Frontiers Media, 2020.","apa":"Beattie, R. J., Hippenmeyer, S., &#38; Pauler, F. (2020). SCOPES: Sparking curiosity through Open-Source platforms in education and science. <i>Frontiers in Education</i>. Frontiers Media. <a href=\"https://doi.org/10.3389/feduc.2020.00048\">https://doi.org/10.3389/feduc.2020.00048</a>","ista":"Beattie RJ, Hippenmeyer S, Pauler F. 2020. SCOPES: Sparking curiosity through Open-Source platforms in education and science. Frontiers in Education. 5, 48.","mla":"Beattie, Robert J., et al. “SCOPES: Sparking Curiosity through Open-Source Platforms in Education and Science.” <i>Frontiers in Education</i>, vol. 5, 48, Frontiers Media, 2020, doi:<a href=\"https://doi.org/10.3389/feduc.2020.00048\">10.3389/feduc.2020.00048</a>.","short":"R.J. Beattie, S. Hippenmeyer, F. Pauler, Frontiers in Education 5 (2020).","chicago":"Beattie, Robert J, Simon Hippenmeyer, and Florian Pauler. “SCOPES: Sparking Curiosity through Open-Source Platforms in Education and Science.” <i>Frontiers in Education</i>. Frontiers Media, 2020. <a href=\"https://doi.org/10.3389/feduc.2020.00048\">https://doi.org/10.3389/feduc.2020.00048</a>.","ama":"Beattie RJ, Hippenmeyer S, Pauler F. SCOPES: Sparking curiosity through Open-Source platforms in education and science. <i>Frontiers in Education</i>. 2020;5. doi:<a href=\"https://doi.org/10.3389/feduc.2020.00048\">10.3389/feduc.2020.00048</a>"},"volume":5,"doi":"10.3389/feduc.2020.00048","day":"08","publisher":"Frontiers Media","type":"journal_article","ec_funded":1,"publication_status":"published","article_type":"original","project":[{"call_identifier":"FWF","name":"Molecular Mechanisms Regulating Gliogenesis in the Neocortex","_id":"264E56E2-B435-11E9-9278-68D0E5697425","grant_number":"M02416"},{"_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780","call_identifier":"H2020","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"}],"author":[{"first_name":"Robert J","full_name":"Beattie, Robert J","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","last_name":"Beattie","orcid":"0000-0002-8483-8753"},{"last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","first_name":"Simon","full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","orcid":"0000-0002-7462-0048","last_name":"Pauler"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file":[{"date_updated":"2020-07-14T12:48:03Z","file_name":"2020_FrontiersEduc_Beattie.pdf","checksum":"a24ec24e38d843341ae620ec76c53688","file_id":"7818","file_size":1402146,"relation":"main_file","content_type":"application/pdf","access_level":"open_access","creator":"dernst","date_created":"2020-05-11T11:34:08Z"}],"oa":1,"date_published":"2020-05-08T00:00:00Z","scopus_import":"1","abstract":[{"text":"Scientific research is to date largely restricted to wealthy laboratories in developed nations due to the necessity of complex and expensive equipment. This inequality limits the capacity of science to be used as a diplomatic channel. Maker movements use open-source technologies including additive manufacturing (3D printing) and laser cutting, together with low-cost computers for developing novel products. This movement is setting the groundwork for a revolution, allowing scientific equipment to be sourced at a fraction of the cost and has the potential to increase the availability of equipment for scientists around the world. Science education is increasingly recognized as another channel for science diplomacy. In this perspective, we introduce the idea that the Maker movement and open-source technologies have the potential to revolutionize science, technology, engineering and mathematics (STEM) education worldwide. We present an open-source STEM didactic tool called SCOPES (Sparking Curiosity through Open-source Platforms in Education and Science). SCOPES is self-contained, independent of local resources, and cost-effective. SCOPES can be adapted to communicate complex subjects from genetics to neurobiology, perform real-world biological experiments and explore digitized scientific samples. We envision such platforms will enhance science diplomacy by providing a means for scientists to share their findings with classrooms and for educators to incorporate didactic concepts into STEM lessons. By providing students the opportunity to design, perform, and share scientific experiments, students also experience firsthand the benefits of a multinational scientific community. We provide instructions on how to build and use SCOPES on our webpage: http://scopeseducation.org.","lang":"eng"}],"status":"public","ddc":["570"],"article_processing_charge":"No","month":"05","_id":"7814","year":"2020","oa_version":"Published Version","title":"SCOPES: Sparking curiosity through Open-Source platforms in education and science"},{"status":"public","abstract":[{"lang":"eng","text":"In mammalian genomes, a subset of genes is regulated by genomic imprinting, resulting in silencing of one parental allele. Imprinting is essential for cerebral cortex development, but prevalence and functional impact in individual cells is unclear. Here, we determined allelic expression in cortical cell types and established a quantitative platform to interrogate imprinting in single cells. We created cells with uniparental chromosome disomy (UPD) containing two copies of either the maternal or the paternal chromosome; hence, imprinted genes will be 2-fold overexpressed or not expressed. By genetic labeling of UPD, we determined cellular phenotypes and transcriptional responses to deregulated imprinted gene expression at unprecedented single-cell resolution. We discovered an unexpected degree of cell-type specificity and a novel function of imprinting in the regulation of cortical astrocyte survival. More generally, our results suggest functional relevance of imprinted gene expression in glial astrocyte lineage and thus for generating cortical cell-type diversity."}],"scopus_import":"1","date_published":"2020-09-23T00:00:00Z","ddc":["570"],"acknowledgement":"We thank A. Heger (IST Austria Preclinical Facility), A. Sommer and C. Czepe (VBCF GmbH, NGS Unit), and A. Seitz and P. Moll (Lexogen GmbH) for technical support; G. Arque, S. Resch, C. Igler, C. Dotter, C. Yahya, Q. Hudson, and D. Andergassen for initial experiments and/or assistance; D. Barlow, O. Bell, and all members of the Hippenmeyer lab for discussion; and N. Barton, B. Vicoso, M. Sixt, and L. Luo for comments on earlier versions of the manuscript. This research was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Bioimaging Facilities (BIF), Life Science Facilities (LSF), and Preclinical Facilities (PCF). A.H.H. is a recipient of a DOC fellowship (24812) of the Austrian Academy of Sciences. N.A. received support from the FWF Firnberg-Programm (T 1031). R.B. received support from the FWF Meitner-Programm (M 2416). This work was also supported by IST Austria institutional funds; a NÖ Forschung und Bildung n[f+b] life science call grant (C13-002) to S.H.; a program grant from the Human Frontiers Science Program (RGP0053/2014) to S.H.; the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement 618444 to S.H.; and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program (grant agreement 725780 LinPro) to S.H.","author":[{"last_name":"Laukoter","orcid":"0000-0002-7903-3010","first_name":"Susanne","full_name":"Laukoter, Susanne","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Pauler","orcid":"0000-0002-7462-0048","first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian"},{"orcid":"0000-0002-8483-8753","last_name":"Beattie","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","full_name":"Beattie, Robert J","first_name":"Robert J"},{"orcid":"0000-0002-3183-8207","last_name":"Amberg","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","full_name":"Amberg, Nicole","first_name":"Nicole"},{"first_name":"Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87","full_name":"Hansen, Andi H","last_name":"Hansen"},{"id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","full_name":"Streicher, Carmen","first_name":"Carmen","last_name":"Streicher"},{"last_name":"Penz","full_name":"Penz, Thomas","first_name":"Thomas"},{"orcid":"0000-0001-6091-3088","last_name":"Bock","first_name":"Christoph","full_name":"Bock, Christoph"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","first_name":"Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"}],"publication_status":"published","article_type":"original","project":[{"name":"Molecular mechanisms of radial neuronal migration","_id":"2625A13E-B435-11E9-9278-68D0E5697425","grant_number":"24812"},{"call_identifier":"FWF","name":"Role of Eed in neural stem cell lineage progression","_id":"268F8446-B435-11E9-9278-68D0E5697425","grant_number":"T01031"},{"name":"Molecular Mechanisms Regulating Gliogenesis in the Neocortex","call_identifier":"FWF","grant_number":"M02416","_id":"264E56E2-B435-11E9-9278-68D0E5697425"},{"grant_number":"LS13-002","_id":"25D92700-B435-11E9-9278-68D0E5697425","name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain"},{"grant_number":"RGP0053/2014","_id":"25D7962E-B435-11E9-9278-68D0E5697425","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level"},{"grant_number":"618444","_id":"25D61E48-B435-11E9-9278-68D0E5697425","name":"Molecular Mechanisms of Cerebral Cortex Development","call_identifier":"FP7"},{"_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780","call_identifier":"H2020","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"}],"oa":1,"isi":1,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file":[{"success":1,"checksum":"7becdc16a6317304304631087ae7dd7f","file_name":"2020_Neuron_Laukoter.pdf","date_updated":"2020-12-02T09:26:46Z","content_type":"application/pdf","date_created":"2020-12-02T09:26:46Z","creator":"dernst","access_level":"open_access","file_id":"8828","file_size":8911830,"relation":"main_file"}],"oa_version":"Published Version","issue":"6","_id":"8162","year":"2020","title":"Cell-type specificity of genomic imprinting in cerebral cortex","article_processing_charge":"No","month":"09","pmid":1,"publication_identifier":{"issn":["0896-6273"]},"language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"       107","corr_author":"1","external_id":{"isi":["000579698700006"],"pmid":["32707083"]},"has_accepted_license":"1","date_updated":"2025-06-12T07:19:46Z","department":[{"_id":"SiHi"}],"file_date_updated":"2020-12-02T09:26:46Z","date_created":"2020-07-23T16:03:12Z","acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"},{"_id":"PreCl"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","short":"CC BY-NC-ND (4.0)"},"volume":107,"citation":{"chicago":"Laukoter, Susanne, Florian Pauler, Robert J Beattie, Nicole Amberg, Andi H Hansen, Carmen Streicher, Thomas Penz, Christoph Bock, and Simon Hippenmeyer. “Cell-Type Specificity of Genomic Imprinting in Cerebral Cortex.” <i>Neuron</i>. Elsevier, 2020. <a href=\"https://doi.org/10.1016/j.neuron.2020.06.031\">https://doi.org/10.1016/j.neuron.2020.06.031</a>.","ama":"Laukoter S, Pauler F, Beattie RJ, et al. Cell-type specificity of genomic imprinting in cerebral cortex. <i>Neuron</i>. 2020;107(6):1160-1179.e9. doi:<a href=\"https://doi.org/10.1016/j.neuron.2020.06.031\">10.1016/j.neuron.2020.06.031</a>","mla":"Laukoter, Susanne, et al. “Cell-Type Specificity of Genomic Imprinting in Cerebral Cortex.” <i>Neuron</i>, vol. 107, no. 6, Elsevier, 2020, p. 1160–1179.e9, doi:<a href=\"https://doi.org/10.1016/j.neuron.2020.06.031\">10.1016/j.neuron.2020.06.031</a>.","ista":"Laukoter S, Pauler F, Beattie RJ, Amberg N, Hansen AH, Streicher C, Penz T, Bock C, Hippenmeyer S. 2020. Cell-type specificity of genomic imprinting in cerebral cortex. Neuron. 107(6), 1160–1179.e9.","apa":"Laukoter, S., Pauler, F., Beattie, R. J., Amberg, N., Hansen, A. H., Streicher, C., … Hippenmeyer, S. (2020). Cell-type specificity of genomic imprinting in cerebral cortex. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2020.06.031\">https://doi.org/10.1016/j.neuron.2020.06.031</a>","ieee":"S. Laukoter <i>et al.</i>, “Cell-type specificity of genomic imprinting in cerebral cortex,” <i>Neuron</i>, vol. 107, no. 6. Elsevier, p. 1160–1179.e9, 2020.","short":"S. Laukoter, F. Pauler, R.J. Beattie, N. Amberg, A.H. Hansen, C. Streicher, T. Penz, C. Bock, S. Hippenmeyer, Neuron 107 (2020) 1160–1179.e9."},"type":"journal_article","ec_funded":1,"related_material":{"link":[{"url":"https://ist.ac.at/en/news/cells-react-differently-to-genomic-imprinting/","relation":"press_release","description":"News on IST Website"}]},"publisher":"Elsevier","doi":"10.1016/j.neuron.2020.06.031","day":"23","page":"1160-1179.e9","publication":"Neuron"},{"year":"2020","_id":"8813","citation":{"short":"L. Santini, F. Halbritter, F. Titz-Teixeira, T. Suzuki, M. Asami, J. Ramesmayer, X. Ma, A. Lackner, N. Warr, F. Pauler, S. Hippenmeyer, E. Laue, M. Farlik, C. Bock, A. Beyer, A.C.F. Perry, M. Leeb, BioRxiv (n.d.).","ieee":"L. Santini <i>et al.</i>, “Novel imprints in mouse blastocysts are predominantly DNA methylation independent,” <i>bioRxiv</i>. Cold Spring Harbor Laboratory.","apa":"Santini, L., Halbritter, F., Titz-Teixeira, F., Suzuki, T., Asami, M., Ramesmayer, J., … Leeb, M. (n.d.). Novel imprints in mouse blastocysts are predominantly DNA methylation independent. <i>bioRxiv</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/2020.11.03.366948\">https://doi.org/10.1101/2020.11.03.366948</a>","mla":"Santini, Laura, et al. “Novel Imprints in Mouse Blastocysts Are Predominantly DNA Methylation Independent.” <i>BioRxiv</i>, Cold Spring Harbor Laboratory, doi:<a href=\"https://doi.org/10.1101/2020.11.03.366948\">10.1101/2020.11.03.366948</a>.","ista":"Santini L, Halbritter F, Titz-Teixeira F, Suzuki T, Asami M, Ramesmayer J, Ma X, Lackner A, Warr N, Pauler F, Hippenmeyer S, Laue E, Farlik M, Bock C, Beyer A, Perry ACF, Leeb M. Novel imprints in mouse blastocysts are predominantly DNA methylation independent. bioRxiv, <a href=\"https://doi.org/10.1101/2020.11.03.366948\">10.1101/2020.11.03.366948</a>.","ama":"Santini L, Halbritter F, Titz-Teixeira F, et al. Novel imprints in mouse blastocysts are predominantly DNA methylation independent. <i>bioRxiv</i>. doi:<a href=\"https://doi.org/10.1101/2020.11.03.366948\">10.1101/2020.11.03.366948</a>","chicago":"Santini, Laura, Florian Halbritter, Fabian Titz-Teixeira, Toru Suzuki, Maki Asami, Julia Ramesmayer, Xiaoyan Ma, et al. “Novel Imprints in Mouse Blastocysts Are Predominantly DNA Methylation Independent.” <i>BioRxiv</i>. Cold Spring Harbor Laboratory, n.d. <a href=\"https://doi.org/10.1101/2020.11.03.366948\">https://doi.org/10.1101/2020.11.03.366948</a>."},"oa_version":"Preprint","doi":"10.1101/2020.11.03.366948","publisher":"Cold Spring Harbor Laboratory","day":"05","title":"Novel imprints in mouse blastocysts are predominantly DNA methylation independent","type":"preprint","publication":"bioRxiv","article_processing_charge":"No","pmid":1,"main_file_link":[{"url":"https://doi.org/10.1101/2020.11.03.366948","open_access":"1"}],"month":"11","abstract":[{"text":"In mammals, chromatin marks at imprinted genes are asymmetrically inherited to control parentally-biased gene expression. This control is thought predominantly to involve parent-specific differentially methylated regions (DMR) in genomic DNA. However, neither parent-of-origin-specific transcription nor DMRs have been comprehensively mapped. We here address this by integrating transcriptomic and epigenomic approaches in mouse preimplantation embryos (blastocysts). Transcriptome-analysis identified 71 genes expressed with previously unknown parent-of-origin-specific expression in blastocysts (nBiX: novel blastocyst-imprinted expression). Uniparental expression of nBiX genes disappeared soon after implantation. Micro-whole-genome bisulfite sequencing (μWGBS) of individual uniparental blastocysts detected 859 DMRs. Only 18% of nBiXs were associated with a DMR, whereas 60% were associated with parentally-biased H3K27me3. This suggests a major role for Polycomb-mediated imprinting in blastocysts. Five nBiX-clusters contained at least one known imprinted gene, and five novel clusters contained exclusively nBiX-genes. These data suggest a complex program of stage-specific imprinting involving different tiers of regulation.","lang":"eng"}],"language":[{"iso":"eng"}],"date_published":"2020-11-05T00:00:00Z","status":"public","date_updated":"2023-09-12T11:05:28Z","external_id":{"pmid":["PPR234457 "]},"date_created":"2020-11-26T07:17:19Z","publication_status":"submitted","author":[{"last_name":"Santini","full_name":"Santini, Laura","first_name":"Laura"},{"last_name":"Halbritter","first_name":"Florian","full_name":"Halbritter, Florian"},{"full_name":"Titz-Teixeira, Fabian","first_name":"Fabian","last_name":"Titz-Teixeira"},{"last_name":"Suzuki","first_name":"Toru","full_name":"Suzuki, Toru"},{"full_name":"Asami, Maki","first_name":"Maki","last_name":"Asami"},{"last_name":"Ramesmayer","first_name":"Julia","full_name":"Ramesmayer, Julia"},{"last_name":"Ma","full_name":"Ma, Xiaoyan","first_name":"Xiaoyan"},{"full_name":"Lackner, Andreas","first_name":"Andreas","last_name":"Lackner"},{"last_name":"Warr","first_name":"Nick","full_name":"Warr, Nick"},{"first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","last_name":"Pauler","orcid":"0000-0002-7462-0048"},{"first_name":"Simon","full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061"},{"last_name":"Laue","full_name":"Laue, Ernest","first_name":"Ernest"},{"full_name":"Farlik, Matthias","first_name":"Matthias","last_name":"Farlik"},{"last_name":"Bock","full_name":"Bock, Christoph","first_name":"Christoph"},{"full_name":"Beyer, Andreas","first_name":"Andreas","last_name":"Beyer"},{"full_name":"Perry, Anthony C. F.","first_name":"Anthony C. F.","last_name":"Perry"},{"last_name":"Leeb","full_name":"Leeb, Martin","first_name":"Martin"}],"department":[{"_id":"SiHi"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","oa":1},{"article_number":"195","department":[{"_id":"SiHi"}],"file_date_updated":"2020-07-14T12:47:54Z","date_created":"2020-01-11T10:42:48Z","acknowledged_ssus":[{"_id":"PreCl"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"publication_identifier":{"issn":["2041-1723"]},"intvolume":"        11","language":[{"iso":"eng"}],"quality_controlled":"1","external_id":{"isi":["000551459000005"],"pmid":["31924768"]},"corr_author":"1","date_updated":"2025-06-12T07:30:49Z","has_accepted_license":"1","publication":"Nature Communications","volume":11,"citation":{"chicago":"Laukoter, Susanne, Robert J Beattie, Florian Pauler, Nicole Amberg, Keiichi I. Nakayama, and Simon Hippenmeyer. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously Promotes Cell Survival in Cerebral Cortex Development.” <i>Nature Communications</i>. Springer Nature, 2020. <a href=\"https://doi.org/10.1038/s41467-019-14077-2\">https://doi.org/10.1038/s41467-019-14077-2</a>.","ama":"Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. <i>Nature Communications</i>. 2020;11. doi:<a href=\"https://doi.org/10.1038/s41467-019-14077-2\">10.1038/s41467-019-14077-2</a>","apa":"Laukoter, S., Beattie, R. J., Pauler, F., Amberg, N., Nakayama, K. I., &#38; Hippenmeyer, S. (2020). Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-019-14077-2\">https://doi.org/10.1038/s41467-019-14077-2</a>","mla":"Laukoter, Susanne, et al. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously Promotes Cell Survival in Cerebral Cortex Development.” <i>Nature Communications</i>, vol. 11, 195, Springer Nature, 2020, doi:<a href=\"https://doi.org/10.1038/s41467-019-14077-2\">10.1038/s41467-019-14077-2</a>.","ista":"Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. 2020. Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. Nature Communications. 11, 195.","ieee":"S. Laukoter, R. J. Beattie, F. Pauler, N. Amberg, K. I. Nakayama, and S. Hippenmeyer, “Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development,” <i>Nature Communications</i>, vol. 11. Springer Nature, 2020.","short":"S. Laukoter, R.J. Beattie, F. Pauler, N. Amberg, K.I. Nakayama, S. Hippenmeyer, Nature Communications 11 (2020)."},"related_material":{"link":[{"description":"News on IST Homepage","relation":"press_release","url":"https://ist.ac.at/en/news/new-function-for-potential-tumour-suppressor-in-brain-development/"}]},"ec_funded":1,"type":"journal_article","publisher":"Springer Nature","day":"10","doi":"10.1038/s41467-019-14077-2","author":[{"orcid":"0000-0002-7903-3010","last_name":"Laukoter","full_name":"Laukoter, Susanne","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","first_name":"Susanne"},{"orcid":"0000-0002-8483-8753","last_name":"Beattie","first_name":"Robert J","full_name":"Beattie, Robert J","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Pauler","orcid":"0000-0002-7462-0048","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","first_name":"Florian"},{"last_name":"Amberg","orcid":"0000-0002-3183-8207","full_name":"Amberg, Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","first_name":"Nicole"},{"first_name":"Keiichi I.","full_name":"Nakayama, Keiichi I.","last_name":"Nakayama"},{"full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"}],"project":[{"_id":"268F8446-B435-11E9-9278-68D0E5697425","grant_number":"T01031","name":"Role of Eed in neural stem cell lineage progression","call_identifier":"FWF"},{"_id":"264E56E2-B435-11E9-9278-68D0E5697425","grant_number":"M02416","call_identifier":"FWF","name":"Molecular Mechanisms Regulating Gliogenesis in the Neocortex"},{"_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780","call_identifier":"H2020","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"},{"_id":"25D92700-B435-11E9-9278-68D0E5697425","grant_number":"LS13-002","name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain"}],"publication_status":"published","article_type":"original","oa":1,"file":[{"creator":"dernst","date_created":"2020-01-13T07:42:31Z","access_level":"open_access","content_type":"application/pdf","relation":"main_file","file_size":8063333,"file_id":"7261","checksum":"ebf1ed522f4e0be8d94c939c1806a709","file_name":"2020_NatureComm_Laukoter.pdf","date_updated":"2020-07-14T12:47:54Z"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","isi":1,"status":"public","scopus_import":"1","abstract":[{"text":"The cyclin-dependent kinase inhibitor p57KIP2 is encoded by the imprinted Cdkn1c locus, exhibits maternal expression, and is essential for cerebral cortex development. How Cdkn1c regulates corticogenesis is however not clear. To this end we employ Mosaic Analysis with Double Markers (MADM) technology to genetically dissect Cdkn1c gene function in corticogenesis at single cell resolution. We find that the previously described growth-inhibitory Cdkn1c function is a non-cell-autonomous one, acting on the whole organism. In contrast we reveal a growth-promoting cell-autonomous Cdkn1c function which at the mechanistic level mediates radial glial progenitor cell and nascent projection neuron survival. Strikingly, the growth-promoting function of Cdkn1c is highly dosage sensitive but not subject to genomic imprinting. Collectively, our results suggest that the Cdkn1c locus regulates cortical development through distinct cell-autonomous and non-cell-autonomous mechanisms. More generally, our study highlights the importance to probe the relative contributions of cell intrinsic gene function and tissue-wide mechanisms to the overall phenotype.","lang":"eng"}],"date_published":"2020-01-10T00:00:00Z","ddc":["570"],"article_processing_charge":"No","month":"01","pmid":1,"oa_version":"Published Version","year":"2020","_id":"7253","title":"Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development"},{"title":"Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy","year":"2020","issue":"3","_id":"8978","oa_version":"Published Version","pmid":1,"month":"12","article_processing_charge":"No","acknowledgement":"This research was supported by the Scientific Service Units (SSU) at IST Austria through resources provided by the Bioimaging (BIF) and Preclinical Facilities (PCF). N.A received support from the FWF Firnberg-Programm (T 1031). This work was also supported by IST Austria institutional funds; FWF SFB F78 to S.H.; NÖ Forschung und Bildung n[f+b] life science call grant (C13-002) to S.H.; the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement no. 618444 to S.H.; and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 725780 LinPro) to S.H.","ddc":["570"],"abstract":[{"text":"Mosaic analysis with double markers (MADM) technology enables concomitant fluorescent cell labeling and induction of uniparental chromosome disomy (UPD) with single-cell resolution. In UPD, imprinted genes are either overexpressed 2-fold or are not expressed. Here, the MADM platform is utilized to probe imprinting phenotypes at the transcriptional level. This protocol highlights major steps for the generation and isolation of projection neurons and astrocytes with MADM-induced UPD from mouse cerebral cortex for downstream single-cell and low-input sample RNA-sequencing experiments.\r\n\r\nFor complete details on the use and execution of this protocol, please refer to Laukoter et al. (2020b).","lang":"eng"}],"scopus_import":"1","date_published":"2020-12-18T00:00:00Z","status":"public","file":[{"date_updated":"2021-01-07T15:57:27Z","file_name":"2020_STARProtocols_Laukoter.pdf","success":1,"checksum":"f1e9a433e9cb0f41f7b6df6b76db1f6e","file_id":"8996","relation":"main_file","file_size":4031449,"content_type":"application/pdf","access_level":"open_access","date_created":"2021-01-07T15:57:27Z","creator":"dernst"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","oa":1,"project":[{"name":"Role of Eed in neural stem cell lineage progression","call_identifier":"FWF","_id":"268F8446-B435-11E9-9278-68D0E5697425","grant_number":"T01031"},{"name":"Stem Cell Modulation in Neural Development and Regeneration/ P05-Molecular Mechanisms of Neural Stem Cell Lineage Progression","_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E","grant_number":"F7805"},{"_id":"25D92700-B435-11E9-9278-68D0E5697425","grant_number":"LS13-002","name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain"},{"_id":"25D61E48-B435-11E9-9278-68D0E5697425","grant_number":"618444","call_identifier":"FP7","name":"Molecular Mechanisms of Cerebral Cortex Development"},{"_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780","call_identifier":"H2020","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"}],"article_type":"original","publication_status":"published","author":[{"id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","full_name":"Laukoter, Susanne","first_name":"Susanne","last_name":"Laukoter","orcid":"0000-0002-7903-3010"},{"last_name":"Amberg","orcid":"0000-0002-3183-8207","first_name":"Nicole","full_name":"Amberg, Nicole","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0002-7462-0048","last_name":"Pauler","first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061"}],"day":"18","publisher":"Elsevier","doi":"10.1016/j.xpro.2020.100215","type":"journal_article","ec_funded":1,"citation":{"ama":"Laukoter S, Amberg N, Pauler F, Hippenmeyer S. Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy. <i>STAR Protocols</i>. 2020;1(3). doi:<a href=\"https://doi.org/10.1016/j.xpro.2020.100215\">10.1016/j.xpro.2020.100215</a>","chicago":"Laukoter, Susanne, Nicole Amberg, Florian Pauler, and Simon Hippenmeyer. “Generation and Isolation of Single Cells from Mouse Brain with Mosaic Analysis with Double Markers-Induced Uniparental Chromosome Disomy.” <i>STAR Protocols</i>. Elsevier, 2020. <a href=\"https://doi.org/10.1016/j.xpro.2020.100215\">https://doi.org/10.1016/j.xpro.2020.100215</a>.","short":"S. Laukoter, N. Amberg, F. Pauler, S. Hippenmeyer, STAR Protocols 1 (2020).","ieee":"S. Laukoter, N. Amberg, F. Pauler, and S. Hippenmeyer, “Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy,” <i>STAR Protocols</i>, vol. 1, no. 3. Elsevier, 2020.","ista":"Laukoter S, Amberg N, Pauler F, Hippenmeyer S. 2020. Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy. STAR Protocols. 1(3), 100215.","apa":"Laukoter, S., Amberg, N., Pauler, F., &#38; Hippenmeyer, S. (2020). Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy. <i>STAR Protocols</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.xpro.2020.100215\">https://doi.org/10.1016/j.xpro.2020.100215</a>","mla":"Laukoter, Susanne, et al. “Generation and Isolation of Single Cells from Mouse Brain with Mosaic Analysis with Double Markers-Induced Uniparental Chromosome Disomy.” <i>STAR Protocols</i>, vol. 1, no. 3, 100215, Elsevier, 2020, doi:<a href=\"https://doi.org/10.1016/j.xpro.2020.100215\">10.1016/j.xpro.2020.100215</a>."},"volume":1,"publication":"STAR Protocols","date_updated":"2025-04-15T08:23:06Z","has_accepted_license":"1","external_id":{"pmid":["33377108"]},"corr_author":"1","intvolume":"         1","quality_controlled":"1","language":[{"iso":"eng"}],"publication_identifier":{"issn":["2666-1667"]},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","short":"CC BY-NC-ND (4.0)"},"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"date_created":"2020-12-30T10:17:07Z","file_date_updated":"2021-01-07T15:57:27Z","article_number":"100215","department":[{"_id":"SiHi"}]},{"corr_author":"1","external_id":{"pmid":["31329595"],"isi":["000478689100025"]},"has_accepted_license":"1","date_updated":"2024-10-09T20:59:14Z","publication_identifier":{"issn":["1553-7404"]},"language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"        15","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"department":[{"_id":"SiHi"}],"article_number":"e1008268","file_date_updated":"2020-07-14T12:47:57Z","date_created":"2020-01-29T16:14:07Z","type":"journal_article","day":"22","publisher":"Public Library of Science","doi":"10.1371/journal.pgen.1008268","volume":15,"citation":{"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.","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>","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.","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).","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>.","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>"},"publication":"PLoS Genetics","ddc":["570"],"status":"public","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"}],"scopus_import":"1","date_published":"2019-07-22T00:00:00Z","oa":1,"isi":1,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file":[{"file_id":"7446","relation":"main_file","file_size":2302307,"content_type":"application/pdf","access_level":"open_access","date_created":"2020-02-04T10:11:55Z","creator":"dernst","date_updated":"2020-07-14T12:47:57Z","file_name":"2019_PlosGenetics_Andergassen.pdf","checksum":"2f51fc91e4a4199827adc51d432ad864"}],"author":[{"full_name":"Andergassen, Daniel","first_name":"Daniel","last_name":"Andergassen"},{"last_name":"Muckenhuber","full_name":"Muckenhuber, Markus","first_name":"Markus"},{"last_name":"Bammer","full_name":"Bammer, Philipp C.","first_name":"Philipp C."},{"full_name":"Kulinski, Tomasz M.","first_name":"Tomasz M.","last_name":"Kulinski"},{"first_name":"Hans-Christian","full_name":"Theussl, Hans-Christian","last_name":"Theussl"},{"full_name":"Shimizu, Takahiko","first_name":"Takahiko","last_name":"Shimizu"},{"last_name":"Penninger","full_name":"Penninger, Josef M.","first_name":"Josef M."},{"first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","orcid":"0000-0002-7462-0048","last_name":"Pauler"},{"full_name":"Hudson, Quanah J.","first_name":"Quanah J.","last_name":"Hudson"}],"publication_status":"published","article_type":"original","title":"The Airn lncRNA does not require any DNA elements within its locus to silence distant imprinted genes","oa_version":"Published Version","issue":"7","_id":"7399","year":"2019","month":"07","pmid":1,"article_processing_charge":"No"},{"language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"        19","publication_identifier":{"issn":["1471-2164"]},"has_accepted_license":"1","date_updated":"2023-09-13T09:10:47Z","external_id":{"isi":["000450976700002"]},"file_date_updated":"2020-07-14T12:45:23Z","date_created":"2018-12-11T11:44:12Z","department":[{"_id":"SiHi"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"citation":{"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>","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>.","short":"J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S. Herzig, M. Scheideler, BMC Genomics 19 (2018).","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.","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>.","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>"},"volume":19,"publisher":"BioMed Central","doi":"10.1186/s12864-018-5173-0","day":"03","type":"journal_article","related_material":{"record":[{"id":"9807","relation":"research_data","status":"public"},{"id":"9808","relation":"research_data","status":"public"}]},"publication":"BMC Genomics","publist_id":"8035","abstract":[{"lang":"eng","text":"Background: Norepinephrine (NE) signaling has a key role in white adipose tissue (WAT) functions, including lipolysis, free fatty acid liberation and, under certain conditions, conversion of white into brite (brown-in-white) adipocytes. However, acute effects of NE stimulation have not been described at the transcriptional network level. Results: We used RNA-seq to uncover a broad transcriptional response. The inference of protein-protein and protein-DNA interaction networks allowed us to identify a set of immediate-early genes (IEGs) with high betweenness, validating our approach and suggesting a hierarchical control of transcriptional regulation. In addition, we identified a transcriptional regulatory network with IEGs as master regulators, including HSF1 and NFIL3 as novel NE-induced IEG candidates. Moreover, a functional enrichment analysis and gene clustering into functional modules suggest a crosstalk between metabolic, signaling, and immune responses. Conclusions: Altogether, our network biology approach explores for the first time the immediate-early systems level response of human adipocytes to acute sympathetic activation, thereby providing a first network basis of early cell fate programs and crosstalks between metabolic and transcriptional networks required for proper WAT function."}],"scopus_import":"1","date_published":"2018-11-03T00:00:00Z","status":"public","ddc":["570"],"acknowledgement":"This work was funded by the German Centre for Diabetes Research (DZD) and the Austrian Science Fund (FWF, P25729-B19).","publication_status":"published","article_type":"original","author":[{"last_name":"Higareda Almaraz","first_name":"Juan","full_name":"Higareda Almaraz, Juan"},{"last_name":"Karbiener","first_name":"Michael","full_name":"Karbiener, Michael"},{"first_name":"Maude","full_name":"Giroud, Maude","last_name":"Giroud"},{"first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","last_name":"Pauler","orcid":"0000-0002-7462-0048"},{"full_name":"Gerhalter, Teresa","first_name":"Teresa","last_name":"Gerhalter"},{"full_name":"Herzig, Stephan","first_name":"Stephan","last_name":"Herzig"},{"last_name":"Scheideler","full_name":"Scheideler, Marcel","first_name":"Marcel"}],"isi":1,"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","file":[{"checksum":"a56516e734dab589dc7f3e1915973b4d","date_updated":"2020-07-14T12:45:23Z","file_name":"2018_BMCGenomics_Higareda.pdf","content_type":"application/pdf","access_level":"open_access","date_created":"2018-12-17T14:52:57Z","creator":"dernst","file_id":"5712","relation":"main_file","file_size":4629784}],"oa":1,"issue":"1","_id":"20","year":"2018","oa_version":"Published Version","title":"Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes","article_processing_charge":"No","month":"11"},{"date_created":"2021-08-06T12:26:53Z","author":[{"full_name":"Higareda Almaraz, Juan","first_name":"Juan","last_name":"Higareda Almaraz"},{"last_name":"Karbiener","full_name":"Karbiener, Michael","first_name":"Michael"},{"last_name":"Giroud","full_name":"Giroud, Maude","first_name":"Maude"},{"orcid":"0000-0002-7462-0048","last_name":"Pauler","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","first_name":"Florian"},{"last_name":"Gerhalter","first_name":"Teresa","full_name":"Gerhalter, Teresa"},{"last_name":"Herzig","full_name":"Herzig, Stephan","first_name":"Stephan"},{"last_name":"Scheideler","first_name":"Marcel","full_name":"Scheideler, Marcel"}],"department":[{"_id":"SiHi"}],"user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","oa":1,"abstract":[{"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).","lang":"eng"}],"date_published":"2018-11-03T00:00:00Z","status":"public","date_updated":"2023-09-13T09:10:47Z","article_processing_charge":"No","main_file_link":[{"url":"https://doi.org/10.6084/m9.figshare.7295339.v1","open_access":"1"}],"month":"11","year":"2018","_id":"9807","citation":{"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>.","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."},"oa_version":"Published Version","publisher":"Springer Nature","day":"03","doi":"10.6084/m9.figshare.7295339.v1","related_material":{"record":[{"status":"public","id":"20","relation":"used_in_publication"}]},"title":"Additional file 1: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes","type":"research_data_reference"}]