[{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2025-08-11T11:49:30Z","scopus_import":"1","external_id":{"pmid":["38165800"],"oaworkID":["34426698 "]},"publication_identifier":{"eissn":["2666-1667"]},"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"oaworkID":1,"article_type":"review","year":"2024","oa_version":"Published Version","volume":5,"publication_status":"epub_ahead","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.xpro.2023.102795"}],"oa":1,"article_number":"102795","date_published":"2024-01-01T00:00:00Z","_id":"14794","abstract":[{"lang":"eng","text":"Mosaic analysis with double markers (MADM) technology enables the sparse labeling of genetically defined neurons. We present a protocol for time-lapse imaging of cortical projection neuron migration in mice using MADM. We describe steps for the isolation, culturing, and 4D imaging of neuronal dynamics in MADM-labeled brain tissue. While this protocol is compatible with other single-cell labeling methods, the MADM approach provides a genetic platform for the functional assessment of cell-autonomous candidate gene function and the relative contribution of non-cell-autonomous effects.\r\n\r\nFor complete details on the use and execution of this protocol, please refer to Hansen et al. (2022),1 Contreras et al. (2021),2 and Amberg and Hippenmeyer (2021).3"}],"issue":"1","article_processing_charge":"Yes","language":[{"iso":"eng"}],"doi":"10.1016/j.xpro.2023.102795","acknowledgement":"We thank Florian Pauler for discussion and his expert technical support. This research was supported by the Scientific Service Units (SSU) at IST Austria through resources provided by the Imaging and Optics Facility (IOF) and Preclinical Facility (PCF). A.H.H. was a recipient of a DOC Fellowship (24812) of the Austrian Academy of Sciences.","related_material":{"link":[{"relation":"software","url":"http://github.com/hippenmeyerlab"}]},"project":[{"name":"Molecular Mechanisms of Radial Neuronal Migration","grant_number":"24812","_id":"2625A13E-B435-11E9-9278-68D0E5697425"}],"pmid":1,"day":"01","author":[{"id":"38853E16-F248-11E8-B48F-1D18A9856A87","first_name":"Andi H","full_name":"Hansen, Andi H","last_name":"Hansen"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","first_name":"Simon","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer"}],"type":"journal_article","citation":{"apa":"Hansen, A. H., &#38; Hippenmeyer, S. (2024). Time-lapse imaging of cortical projection neuron migration in mice using mosaic analysis with double markers. <i>STAR Protocols</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.xpro.2023.102795\">https://doi.org/10.1016/j.xpro.2023.102795</a>","ama":"Hansen AH, Hippenmeyer S. Time-lapse imaging of cortical projection neuron migration in mice using mosaic analysis with double markers. <i>STAR Protocols</i>. 2024;5(1). doi:<a href=\"https://doi.org/10.1016/j.xpro.2023.102795\">10.1016/j.xpro.2023.102795</a>","short":"A.H. Hansen, S. Hippenmeyer, STAR Protocols 5 (2024).","mla":"Hansen, Andi H., and Simon Hippenmeyer. “Time-Lapse Imaging of Cortical Projection Neuron Migration in Mice Using Mosaic Analysis with Double Markers.” <i>STAR Protocols</i>, vol. 5, no. 1, 102795, Elsevier, 2024, doi:<a href=\"https://doi.org/10.1016/j.xpro.2023.102795\">10.1016/j.xpro.2023.102795</a>.","ista":"Hansen AH, Hippenmeyer S. 2024. Time-lapse imaging of cortical projection neuron migration in mice using mosaic analysis with double markers. STAR Protocols. 5(1), 102795.","ieee":"A. H. Hansen and S. Hippenmeyer, “Time-lapse imaging of cortical projection neuron migration in mice using mosaic analysis with double markers,” <i>STAR Protocols</i>, vol. 5, no. 1. Elsevier, 2024.","chicago":"Hansen, Andi H, and Simon Hippenmeyer. “Time-Lapse Imaging of Cortical Projection Neuron Migration in Mice Using Mosaic Analysis with Double Markers.” <i>STAR Protocols</i>. Elsevier, 2024. <a href=\"https://doi.org/10.1016/j.xpro.2023.102795\">https://doi.org/10.1016/j.xpro.2023.102795</a>."},"title":"Time-lapse imaging of cortical projection neuron migration in mice using mosaic analysis with double markers","quality_controlled":"1","department":[{"_id":"SiHi"}],"publication":"STAR Protocols","status":"public","intvolume":"         5","publisher":"Elsevier","month":"01","date_created":"2024-01-14T23:00:56Z"},{"author":[{"orcid":"0000-0001-8457-2572","id":"471195F6-F248-11E8-B48F-1D18A9856A87","full_name":"Cheung, Giselle T","first_name":"Giselle T","last_name":"Cheung"},{"full_name":"Pauler, Florian","first_name":"Florian","last_name":"Pauler","orcid":"0000-0002-7462-0048","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Koppensteiner, Peter","first_name":"Peter","last_name":"Koppensteiner","orcid":"0000-0002-3509-1948","id":"3B8B25A8-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Krausgruber","full_name":"Krausgruber, Thomas","first_name":"Thomas"},{"id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","last_name":"Streicher","first_name":"Carmen","full_name":"Streicher, Carmen"},{"last_name":"Schrammel","first_name":"Martin","full_name":"Schrammel, Martin","id":"f13e7cae-e8bd-11ed-841a-96dedf69f46d"},{"id":"e68ece33-f6e0-11ea-865d-ae1031dcc090","first_name":"Natalie Y","full_name":"Özgen, Natalie Y","last_name":"Özgen"},{"full_name":"Ivec, Alexis","first_name":"Alexis","last_name":"Ivec","id":"1d144691-e8be-11ed-9b33-bdd3077fad4c"},{"last_name":"Bock","full_name":"Bock, Christoph","first_name":"Christoph"},{"last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi","first_name":"Ryuichi","orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","first_name":"Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"type":"journal_article","day":"17","title":"Multipotent progenitors instruct ontogeny of the superior colliculus","doi":"10.1016/j.neuron.2023.11.009","ddc":["570"],"language":[{"iso":"eng"}],"project":[{"grant_number":"F07805","name":"Molecular Mechanisms of Neural Stem Cell Lineage Progression","_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E"}],"pmid":1,"related_material":{"link":[{"url":"https://ista.ac.at/en/news/the-pedigree-of-brain-cells/","description":"News on ISTA Website","relation":"press_release"}]},"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. ","date_created":"2023-04-27T09:41:48Z","month":"01","page":"230-246.e11","intvolume":"       112","status":"public","publication":"Neuron","department":[{"_id":"SiHi"},{"_id":"RySh"}],"quality_controlled":"1","publisher":"Elsevier","year":"2024","oa_version":"Published Version","has_accepted_license":"1","article_type":"comment","publication_identifier":{"eisbn":["1234995621"],"issn":["0896-6273"],"issnl":["1234-5678"]},"acknowledged_ssus":[{"_id":"Bio"},{"_id":"M-Shop"},{"_id":"LifeSc"},{"_id":"PreCl"}],"external_id":{"pmid":["38096816"]},"scopus_import":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2025-05-14T09:39:37Z","_id":"12875","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"}],"date_published":"2024-01-17T00:00:00Z","file":[{"date_created":"2024-02-06T13:56:15Z","success":1,"content_type":"application/pdf","file_id":"14944","relation":"main_file","checksum":"32b3788f7085cf44a84108d8faaff3ce","date_updated":"2024-02-06T13:56:15Z","access_level":"open_access","file_name":"2024_Neuron_Cheung.pdf","file_size":5942467,"creator":"dernst"}],"article_processing_charge":"Yes (via OA deal)","issue":"2","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"volume":112,"file_date_updated":"2024-02-06T13:56:15Z","oa":1,"publication_status":"published"},{"title":"Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway","citation":{"mla":"Bose, Mahima, et al. “Dual Role of FOXG1 in Regulating Gliogenesis in the Developing Neocortex via the FGF Signalling Pathway.” <i>BioRxiv</i>, Cold Spring Harbor Laboratory, doi:<a href=\"https://doi.org/10.1101/2023.11.30.569337\">10.1101/2023.11.30.569337</a>.","ista":"Bose M, Suresh V, Mishra U, Talwar I, Yadav A, Biswas S, Hippenmeyer S, Tole S. Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway. bioRxiv, <a href=\"https://doi.org/10.1101/2023.11.30.569337\">10.1101/2023.11.30.569337</a>.","ieee":"M. Bose <i>et al.</i>, “Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway,” <i>bioRxiv</i>. Cold Spring Harbor Laboratory.","chicago":"Bose, Mahima, Varun Suresh, Urvi Mishra, Ishita Talwar, Anuradha Yadav, Shiona Biswas, Simon Hippenmeyer, and Shubha Tole. “Dual Role of FOXG1 in Regulating Gliogenesis in the Developing Neocortex via the FGF Signalling Pathway.” <i>BioRxiv</i>. Cold Spring Harbor Laboratory, n.d. <a href=\"https://doi.org/10.1101/2023.11.30.569337\">https://doi.org/10.1101/2023.11.30.569337</a>.","apa":"Bose, M., Suresh, V., Mishra, U., Talwar, I., Yadav, A., Biswas, S., … Tole, S. (n.d.). Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway. <i>bioRxiv</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/2023.11.30.569337\">https://doi.org/10.1101/2023.11.30.569337</a>","ama":"Bose M, Suresh V, Mishra U, et al. Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway. <i>bioRxiv</i>. doi:<a href=\"https://doi.org/10.1101/2023.11.30.569337\">10.1101/2023.11.30.569337</a>","short":"M. Bose, V. Suresh, U. Mishra, I. Talwar, A. Yadav, S. Biswas, S. Hippenmeyer, S. Tole, BioRxiv (n.d.)."},"author":[{"last_name":"Bose","first_name":"Mahima","full_name":"Bose, Mahima"},{"last_name":"Suresh","first_name":"Varun","full_name":"Suresh, Varun"},{"first_name":"Urvi","full_name":"Mishra, Urvi","last_name":"Mishra"},{"full_name":"Talwar, Ishita","first_name":"Ishita","last_name":"Talwar"},{"first_name":"Anuradha","full_name":"Yadav, Anuradha","last_name":"Yadav"},{"full_name":"Biswas, Shiona","first_name":"Shiona","last_name":"Biswas"},{"last_name":"Hippenmeyer","first_name":"Simon","full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061"},{"full_name":"Tole, Shubha","first_name":"Shubha","last_name":"Tole"}],"type":"preprint","year":"2023","oa_version":"Preprint","day":"01","acknowledgement":"We thank Dr. Shital Suryavanshi and the animal house staff of the Tata Institute of\r\nFundamental Research (TIFR) for their excellent support; Gord Fishell and Goichi Miyoshi for\r\nthe Foxg1 floxed mouse line; Hiroshi Kawasaki for the plasmids pCAG-FGF8 and pCAGsFGFR3c. We thank Prof. S.K. Lee for the Foxg1lox/lox genotyping primers and protocol. We thank Dr. Deepak Modi and Dr. Vainav Patel for allowing us to use the NIRRCH FACS Facility and the staff of the NIRRCH and TIFR FACS facilities for their assistance.\r\nWe thank Denis Jabaudon for his critical comments on the manuscript and members of the\r\nJabaudon lab for helpful discussions. This work was funded by the Department of Atomic\r\nEnergy (DAE), Govt. of India (Project Identification no. RTI4003, DAE OM no.\r\n1303/2/2019/R&D-II/DAE/2079).","doi":"10.1101/2023.11.30.569337","date_updated":"2023-12-11T07:37:17Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","language":[{"iso":"eng"}],"article_processing_charge":"No","_id":"14647","date_created":"2023-12-06T13:07:01Z","abstract":[{"text":"In the developing vertebrate central nervous system, neurons and glia typically arise sequentially from common progenitors. Here, we report that the transcription factor Forkhead Box G1 (Foxg1) regulates gliogenesis in the mouse neocortex via distinct cell-autonomous roles in progenitors and in postmitotic neurons that regulate different aspects of the gliogenic FGF signalling pathway. We demonstrate that loss of Foxg1 in cortical progenitors at neurogenic stages causes premature astrogliogenesis. We identify a novel FOXG1 target, the pro-gliogenic FGF pathway component Fgfr3, which is suppressed by FOXG1 cell-autonomously to maintain neurogenesis. Furthermore, FOXG1 can also suppress premature astrogliogenesis triggered by the augmentation of FGF signalling. We identify a second novel function of FOXG1 in regulating the expression of gliogenic ligand FGF18 in new born neocortical upper-layer neurons. Loss of FOXG1 in postmitotic neurons increases Fgf18 expression and enhances gliogenesis in the progenitors. These results fit well with the model that new born neurons secrete cues that trigger progenitors to produce the next wave of cell types, astrocytes. If FGF signalling is attenuated in Foxg1 null progenitors, they progress to oligodendrocyte production. Therefore, loss of FOXG1 transitions the progenitor to a gliogenic state, producing either astrocytes or oligodendrocytes depending on FGF signalling levels. Our results uncover how FOXG1 integrates extrinsic signalling via the FGF pathway to regulate the sequential generation of neurons, astrocytes, and oligodendrocytes in the cerebral cortex.","lang":"eng"}],"date_published":"2023-12-01T00:00:00Z","month":"12","oa":1,"main_file_link":[{"url":"https://doi.org/10.1101/2023.11.30.569337","open_access":"1"}],"publisher":"Cold Spring Harbor Laboratory","publication_status":"submitted","status":"public","publication":"bioRxiv","department":[{"_id":"SiHi"}]},{"status":"public","intvolume":"         5","department":[{"_id":"SiHi"}],"quality_controlled":"1","publication":"STAR Protocols","publisher":"Elsevier","date_created":"2023-12-13T11:48:05Z","month":"12","doi":"10.1016/j.xpro.2023.102771","ddc":["570"],"language":[{"iso":"eng"}],"keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Neuroscience"],"acknowledgement":"This research was supported by the Scientific Service Units (SSU) at IST Austria through resources provided by the Imaging & Optics Facility (IOF) and Preclinical Facilities (PCF). N.A. received support from FWF Firnberg-Programme (T 1031). G.C. received support from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 754411 as an ISTplus postdoctoral fellow. This work was also supported by IST Austria institutional funds, FWF SFB F78 to S.H., and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 725780 LinPro) to S.H.","project":[{"call_identifier":"FWF","_id":"268F8446-B435-11E9-9278-68D0E5697425","name":"Role of Eed in neural stem cell lineage progression","grant_number":"T0101031"},{"call_identifier":"H2020","_id":"260C2330-B435-11E9-9278-68D0E5697425","grant_number":"754411","name":"ISTplus - Postdoctoral Fellowships"},{"grant_number":"F07805","name":"Molecular Mechanisms of Neural Stem Cell Lineage Progression","_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E"},{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}],"pmid":1,"author":[{"orcid":"0000-0002-3183-8207","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","first_name":"Nicole","full_name":"Amberg, Nicole","last_name":"Amberg"},{"first_name":"Giselle T","full_name":"Cheung, Giselle T","last_name":"Cheung","orcid":"0000-0001-8457-2572","id":"471195F6-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","first_name":"Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"type":"journal_article","day":"08","title":"Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry","ec_funded":1,"citation":{"mla":"Amberg, Nicole, et al. “Protocol for Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers by Flow Cytometry.” <i>STAR Protocols</i>, vol. 5, no. 1, 102771, Elsevier, 2023, doi:<a href=\"https://doi.org/10.1016/j.xpro.2023.102771\">10.1016/j.xpro.2023.102771</a>.","chicago":"Amberg, Nicole, Giselle T Cheung, and Simon Hippenmeyer. “Protocol for Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers by Flow Cytometry.” <i>STAR Protocols</i>. Elsevier, 2023. <a href=\"https://doi.org/10.1016/j.xpro.2023.102771\">https://doi.org/10.1016/j.xpro.2023.102771</a>.","ista":"Amberg N, Cheung GT, Hippenmeyer S. 2023. Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols. 5(1), 102771.","ieee":"N. Amberg, G. T. Cheung, and S. Hippenmeyer, “Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry,” <i>STAR Protocols</i>, vol. 5, no. 1. Elsevier, 2023.","ama":"Amberg N, Cheung GT, Hippenmeyer S. Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. <i>STAR Protocols</i>. 2023;5(1). doi:<a href=\"https://doi.org/10.1016/j.xpro.2023.102771\">10.1016/j.xpro.2023.102771</a>","apa":"Amberg, N., Cheung, G. T., &#38; Hippenmeyer, S. (2023). Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. <i>STAR Protocols</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.xpro.2023.102771\">https://doi.org/10.1016/j.xpro.2023.102771</a>","short":"N. Amberg, G.T. Cheung, S. Hippenmeyer, STAR Protocols 5 (2023)."},"volume":5,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"oa":1,"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.xpro.2023.102771"}],"publication_status":"epub_ahead","_id":"14683","abstract":[{"lang":"eng","text":"Mosaic analysis with double markers (MADM) technology enables the generation of genetic mosaic tissue in mice and high-resolution phenotyping at the individual cell level. Here, we present a protocol for isolating MADM-labeled cells with high yield for downstream molecular analyses using fluorescence-activated cell sorting (FACS). We describe steps for generating MADM-labeled mice, perfusion, single-cell suspension, and debris removal. We then detail procedures for cell sorting by FACS and downstream analysis. This protocol is suitable for embryonic to adult mice.\r\nFor complete details on the use and execution of this protocol, please refer to Contreras et al. (2021).1"}],"date_published":"2023-12-08T00:00:00Z","article_number":"102771","issue":"1","article_processing_charge":"No","acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"publication_identifier":{"issn":["2666-1667"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2023-12-18T08:06:14Z","external_id":{"pmid":["38070137"]},"scopus_import":"1","year":"2023","oa_version":"Submitted Version","article_type":"review"},{"abstract":[{"text":"The cerebral cortex is comprised of a vast cell-type diversity sequentially generated by cortical progenitor cells. Faithful progenitor lineage progression requires the tight orchestration of distinct molecular and cellular mechanisms regulating proper progenitor proliferation behavior and differentiation. Correct execution of developmental programs involves a complex interplay of cell intrinsic and tissue-wide mechanisms. Many studies over the past decades have been able to determine a plethora of genes critically involved in cortical development. However, only a few made use of genetic paradigms with sparse and global gene deletion to probe cell-autonomous vs. tissue-wide contribution. In this chapter, we will elaborate on the importance of dissecting the cell-autonomous and tissue-wide mechanisms to gain a precise understanding of gene function during radial glial progenitor lineage progression.","lang":"eng"}],"_id":"14757","date_published":"2023-08-08T00:00:00Z","date_created":"2024-01-08T13:16:36Z","month":"08","article_processing_charge":"No","page":"169-191","status":"public","publication":"Neocortical Neurogenesis in Development and Evolution","quality_controlled":"1","department":[{"_id":"SiHi"}],"publisher":"Wiley","publication_status":"published","type":"book_chapter","author":[{"first_name":"Ana","full_name":"Villalba Requena, Ana","last_name":"Villalba Requena","id":"68cb85a0-39f7-11eb-9559-9aaab4f6a247","orcid":"0000-0002-5615-5277"},{"last_name":"Amberg","first_name":"Nicole","full_name":"Amberg, Nicole","orcid":"0000-0002-3183-8207","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Hippenmeyer","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"year":"2023","oa_version":"None","day":"08","title":"Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression","editor":[{"first_name":"Wieland","full_name":"Huttner, Wieland","last_name":"Huttner"}],"citation":{"short":"A. Villalba Requena, N. Amberg, S. Hippenmeyer, in:, W. Huttner (Ed.), Neocortical Neurogenesis in Development and Evolution, Wiley, 2023, pp. 169–191.","ama":"Villalba Requena A, Amberg N, Hippenmeyer S. Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression. In: Huttner W, ed. <i>Neocortical Neurogenesis in Development and Evolution</i>. Wiley; 2023:169-191. doi:<a href=\"https://doi.org/10.1002/9781119860914.ch10\">10.1002/9781119860914.ch10</a>","apa":"Villalba Requena, A., Amberg, N., &#38; Hippenmeyer, S. (2023). Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression. In W. Huttner (Ed.), <i>Neocortical Neurogenesis in Development and Evolution</i> (pp. 169–191). Wiley. <a href=\"https://doi.org/10.1002/9781119860914.ch10\">https://doi.org/10.1002/9781119860914.ch10</a>","chicago":"Villalba Requena, Ana, Nicole Amberg, and Simon Hippenmeyer. “Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression.” In <i>Neocortical Neurogenesis in Development and Evolution</i>, edited by Wieland Huttner, 169–91. Wiley, 2023. <a href=\"https://doi.org/10.1002/9781119860914.ch10\">https://doi.org/10.1002/9781119860914.ch10</a>.","ista":"Villalba Requena A, Amberg N, Hippenmeyer S. 2023.Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression. In: Neocortical Neurogenesis in Development and Evolution. , 169–191.","ieee":"A. Villalba Requena, N. Amberg, and S. Hippenmeyer, “Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression,” in <i>Neocortical Neurogenesis in Development and Evolution</i>, W. Huttner, Ed. Wiley, 2023, pp. 169–191.","mla":"Villalba Requena, Ana, et al. “Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression.” <i>Neocortical Neurogenesis in Development and Evolution</i>, edited by Wieland Huttner, Wiley, 2023, pp. 169–91, doi:<a href=\"https://doi.org/10.1002/9781119860914.ch10\">10.1002/9781119860914.ch10</a>."},"publication_identifier":{"eisbn":["9781119860914"]},"doi":"10.1002/9781119860914.ch10","scopus_import":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2024-01-09T09:46:57Z","language":[{"iso":"eng"}]},{"volume":111,"publication_status":"published","date_published":"2023-02-01T00:00:00Z","_id":"12542","abstract":[{"lang":"eng","text":"In this issue of Neuron, Espinosa-Medina et al.1 present the TEMPO (Temporal Encoding and Manipulation in a Predefined Order) system, which enables the marking and genetic manipulation of sequentially generated cell lineages in vertebrate species in vivo."}],"article_processing_charge":"No","issue":"3","publication_identifier":{"eissn":["1097-4199"]},"scopus_import":"1","external_id":{"isi":["000994473300001"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","date_updated":"2023-08-01T13:10:27Z","year":"2023","oa_version":"None","article_type":"letter_note","intvolume":"       111","status":"public","publication":"Neuron","quality_controlled":"1","department":[{"_id":"SiHi"}],"isi":1,"publisher":"Elsevier","date_created":"2023-02-12T23:00:58Z","month":"02","page":"291-293","doi":"10.1016/j.neuron.2023.01.006","language":[{"iso":"eng"}],"author":[{"last_name":"Villalba Requena","full_name":"Villalba Requena, Ana","first_name":"Ana","id":"68cb85a0-39f7-11eb-9559-9aaab4f6a247","orcid":"0000-0002-5615-5277"},{"first_name":"Simon","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061"}],"type":"journal_article","day":"01","title":"Going back in time with TEMPO","citation":{"ama":"Villalba Requena A, Hippenmeyer S. Going back in time with TEMPO. <i>Neuron</i>. 2023;111(3):291-293. doi:<a href=\"https://doi.org/10.1016/j.neuron.2023.01.006\">10.1016/j.neuron.2023.01.006</a>","apa":"Villalba Requena, A., &#38; Hippenmeyer, S. (2023). Going back in time with TEMPO. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2023.01.006\">https://doi.org/10.1016/j.neuron.2023.01.006</a>","short":"A. Villalba Requena, S. Hippenmeyer, Neuron 111 (2023) 291–293.","mla":"Villalba Requena, Ana, and Simon Hippenmeyer. “Going Back in Time with TEMPO.” <i>Neuron</i>, vol. 111, no. 3, Elsevier, 2023, pp. 291–93, doi:<a href=\"https://doi.org/10.1016/j.neuron.2023.01.006\">10.1016/j.neuron.2023.01.006</a>.","chicago":"Villalba Requena, Ana, and Simon Hippenmeyer. “Going Back in Time with TEMPO.” <i>Neuron</i>. Elsevier, 2023. <a href=\"https://doi.org/10.1016/j.neuron.2023.01.006\">https://doi.org/10.1016/j.neuron.2023.01.006</a>.","ista":"Villalba Requena A, Hippenmeyer S. 2023. Going back in time with TEMPO. Neuron. 111(3), 291–293.","ieee":"A. Villalba Requena and S. Hippenmeyer, “Going back in time with TEMPO,” <i>Neuron</i>, vol. 111, no. 3. Elsevier, pp. 291–293, 2023."}},{"article_type":"original","oa_version":"None","year":"2023","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","date_updated":"2023-09-05T12:13:34Z","external_id":{"isi":["000957721600001"],"pmid":["36695533"]},"publication_identifier":{"issn":["0022-3077"],"eissn":["1522-1598"]},"issue":"3","article_processing_charge":"No","abstract":[{"lang":"eng","text":"Presynaptic inputs determine the pattern of activation of postsynaptic neurons in a neural circuit. Molecular and genetic pathways that regulate the selective formation of subsets of presynaptic inputs are largely unknown, despite significant understanding of the general process of synaptogenesis. In this study, we have begun to identify such factors using the spinal monosynaptic stretch reflex circuit as a model system. In this neuronal circuit, Ia proprioceptive afferents establish monosynaptic connections with spinal motor neurons that project to the same muscle (termed homonymous connections) or muscles with related or synergistic function. However, monosynaptic connections are not formed with motor neurons innervating muscles with antagonistic functions. The ETS transcription factor ER81 (also known as ETV1) is expressed by all proprioceptive afferents, but only a small set of motor neuron pools in the lumbar spinal cord of the mouse. Here we use conditional mouse genetic techniques to eliminate Er81 expression selectively from motor neurons. We find that ablation of Er81 in motor neurons reduces synaptic inputs from proprioceptive afferents conveying information from homonymous and synergistic muscles, with no change observed in the connectivity pattern from antagonistic proprioceptive afferents. In summary, these findings suggest a role for ER81 in defined motor neuron pools to control the assembly of specific presynaptic inputs and thereby influence the profile of activation of these motor neurons."}],"_id":"12562","date_published":"2023-03-01T00:00:00Z","publication_status":"published","volume":129,"citation":{"short":"D.R. Ladle, S. Hippenmeyer, Journal of Neurophysiology 129 (2023) 501–512.","ama":"Ladle DR, Hippenmeyer S. Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons. <i>Journal of Neurophysiology</i>. 2023;129(3):501-512. doi:<a href=\"https://doi.org/10.1152/jn.00172.2022\">10.1152/jn.00172.2022</a>","apa":"Ladle, D. R., &#38; Hippenmeyer, S. (2023). Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons. <i>Journal of Neurophysiology</i>. American Physiological Society. <a href=\"https://doi.org/10.1152/jn.00172.2022\">https://doi.org/10.1152/jn.00172.2022</a>","chicago":"Ladle, David R., and Simon Hippenmeyer. “Loss of ETV1/ER81 in Motor Neurons Leads to Reduced Monosynaptic Inputs from Proprioceptive Sensory Neurons.” <i>Journal of Neurophysiology</i>. American Physiological Society, 2023. <a href=\"https://doi.org/10.1152/jn.00172.2022\">https://doi.org/10.1152/jn.00172.2022</a>.","ieee":"D. R. Ladle and S. Hippenmeyer, “Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons,” <i>Journal of Neurophysiology</i>, vol. 129, no. 3. American Physiological Society, pp. 501–512, 2023.","ista":"Ladle DR, Hippenmeyer S. 2023. Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons. Journal of Neurophysiology. 129(3), 501–512.","mla":"Ladle, David R., and Simon Hippenmeyer. “Loss of ETV1/ER81 in Motor Neurons Leads to Reduced Monosynaptic Inputs from Proprioceptive Sensory Neurons.” <i>Journal of Neurophysiology</i>, vol. 129, no. 3, American Physiological Society, 2023, pp. 501–12, doi:<a href=\"https://doi.org/10.1152/jn.00172.2022\">10.1152/jn.00172.2022</a>."},"title":"Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons","day":"01","type":"journal_article","author":[{"first_name":"David R.","full_name":"Ladle, David R.","last_name":"Ladle"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","first_name":"Simon","last_name":"Hippenmeyer"}],"acknowledgement":"The authors gratefully thank Dr. Silvia Arber, University of Basel and Friedrich Miescher Institute for Biomedical Research, for support and in whose lab the data were collected. For advice on statistical analysis, we thank Michael Bottomley from the Statistical Consulting Center, College of Science and Mathematics, Wright State University.","pmid":1,"language":[{"iso":"eng"}],"keyword":["Physiology","General Neuroscience"],"doi":"10.1152/jn.00172.2022","page":"501-512","month":"03","date_created":"2023-02-15T14:46:14Z","publisher":"American Physiological Society","isi":1,"department":[{"_id":"SiHi"}],"quality_controlled":"1","publication":"Journal of Neurophysiology","status":"public","intvolume":"       129"},{"acknowledgement":"I wish to thank all current and past members of the Hippenmeyer laboratory at ISTA for exciting discussions on the subject of this review. I apologize to colleagues whose work I could not cite and/or discuss in the frame of the available space. Work in the Hippenmeyer laboratory on the\r\ndiscussed topic is supported by ISTA institutional funds, FWF SFB F78 to S.H., and the European Research Council (ERC) under the European Union’s Horizon 2020 Research and Innovation Programme (grant agree-ment no. 725780 LinPro) to SH.","project":[{"name":"Molecular Mechanisms of Neural Stem Cell Lineage Progression","grant_number":"F07805","_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E"},{"call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"}],"pmid":1,"ddc":["570"],"doi":"10.1016/j.conb.2023.102695","language":[{"iso":"eng"}],"keyword":["General Neuroscience"],"title":"Principles of neural stem cell lineage progression: Insights from developing cerebral cortex","ec_funded":1,"citation":{"ieee":"S. Hippenmeyer, “Principles of neural stem cell lineage progression: Insights from developing cerebral cortex,” <i>Current Opinion in Neurobiology</i>, vol. 79, no. 4. Elsevier, 2023.","ista":"Hippenmeyer S. 2023. Principles of neural stem cell lineage progression: Insights from developing cerebral cortex. Current Opinion in Neurobiology. 79(4), 102695.","chicago":"Hippenmeyer, Simon. “Principles of Neural Stem Cell Lineage Progression: Insights from Developing Cerebral Cortex.” <i>Current Opinion in Neurobiology</i>. Elsevier, 2023. <a href=\"https://doi.org/10.1016/j.conb.2023.102695\">https://doi.org/10.1016/j.conb.2023.102695</a>.","mla":"Hippenmeyer, Simon. “Principles of Neural Stem Cell Lineage Progression: Insights from Developing Cerebral Cortex.” <i>Current Opinion in Neurobiology</i>, vol. 79, no. 4, 102695, Elsevier, 2023, doi:<a href=\"https://doi.org/10.1016/j.conb.2023.102695\">10.1016/j.conb.2023.102695</a>.","short":"S. Hippenmeyer, Current Opinion in Neurobiology 79 (2023).","apa":"Hippenmeyer, S. (2023). Principles of neural stem cell lineage progression: Insights from developing cerebral cortex. <i>Current Opinion in Neurobiology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.conb.2023.102695\">https://doi.org/10.1016/j.conb.2023.102695</a>","ama":"Hippenmeyer S. Principles of neural stem cell lineage progression: Insights from developing cerebral cortex. <i>Current Opinion in Neurobiology</i>. 2023;79(4). doi:<a href=\"https://doi.org/10.1016/j.conb.2023.102695\">10.1016/j.conb.2023.102695</a>"},"author":[{"full_name":"Hippenmeyer, Simon","first_name":"Simon","last_name":"Hippenmeyer","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"type":"journal_article","day":"01","isi":1,"publisher":"Elsevier","intvolume":"        79","status":"public","department":[{"_id":"SiHi"}],"quality_controlled":"1","publication":"Current Opinion in Neurobiology","date_created":"2023-02-26T12:24:21Z","month":"04","publication_identifier":{"issn":["0959-4388"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2023-08-16T12:30:25Z","external_id":{"pmid":["36842274"],"isi":["000953497700001"]},"scopus_import":"1","oa_version":"Published Version","year":"2023","has_accepted_license":"1","article_type":"review","oa":1,"publication_status":"published","volume":79,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"file_date_updated":"2023-08-16T12:29:06Z","issue":"4","article_processing_charge":"Yes (via OA deal)","abstract":[{"lang":"eng","text":"How to generate a brain of correct size and with appropriate cell-type diversity during development is a major question in Neuroscience. In the developing neocortex, radial glial progenitor (RGP) cells are the main neural stem cells that produce cortical excitatory projection neurons, glial cells, and establish the prospective postnatal stem cell niche in the lateral ventricles. RGPs follow a tightly orchestrated developmental program that when disrupted can result in severe cortical malformations such as microcephaly and megalencephaly. The precise cellular and molecular mechanisms instructing faithful RGP lineage progression are however not well understood. This review will summarize recent conceptual advances that contribute to our understanding of the general principles of RGP lineage progression."}],"_id":"12679","date_published":"2023-04-01T00:00:00Z","article_number":"102695","file":[{"access_level":"open_access","date_updated":"2023-08-16T12:29:06Z","checksum":"4d11c4ca87e6cbc4d2ac46d3225ea615","file_size":1787894,"creator":"dernst","file_name":"2023_CurrentOpinionNeurobio_Hippenmeyer.pdf","success":1,"date_created":"2023-08-16T12:29:06Z","file_id":"14071","relation":"main_file","content_type":"application/pdf"}]},{"publication_identifier":{"issn":["0092-8674"]},"acknowledged_ssus":[{"_id":"PreCl"},{"_id":"EM-Fac"},{"_id":"Bio"},{"_id":"LifeSc"}],"scopus_import":"1","external_id":{"isi":["000991468700001"]},"date_updated":"2024-02-07T08:03:32Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","has_accepted_license":"1","year":"2023","oa_version":"Published Version","article_type":"original","oa":1,"publication_status":"published","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"volume":186,"file_date_updated":"2023-05-02T09:26:21Z","article_processing_charge":"Yes (via OA deal)","issue":"9","_id":"12802","abstract":[{"lang":"eng","text":"Little is known about the critical metabolic changes that neural cells have to undergo during development and how temporary shifts in this program can influence brain circuitries and behavior. Inspired by the discovery that mutations in SLC7A5, a transporter of metabolically essential large neutral amino acids (LNAAs), lead to autism, we employed metabolomic profiling to study the metabolic states of the cerebral cortex across different developmental stages. We found that the forebrain undergoes significant metabolic remodeling throughout development, with certain groups of metabolites showing stage-specific changes, but what are the consequences of perturbing this metabolic program? By manipulating Slc7a5 expression in neural cells, we found that the metabolism of LNAAs and lipids are interconnected in the cortex. Deletion of Slc7a5 in neurons affects the postnatal metabolic state, leading to a shift in lipid metabolism. Additionally, it causes stage- and cell-type-specific alterations in neuronal activity patterns, resulting in a long-term circuit dysfunction."}],"date_published":"2023-04-27T00:00:00Z","file":[{"file_id":"12889","relation":"main_file","content_type":"application/pdf","success":1,"date_created":"2023-05-02T09:26:21Z","creator":"dernst","file_size":15712841,"file_name":"2023_Cell_Knaus.pdf","access_level":"open_access","date_updated":"2023-05-02T09:26:21Z","checksum":"47e94fbe19e86505b429cb7a5b503ce6"}],"project":[{"call_identifier":"FWF","_id":"2548AE96-B435-11E9-9278-68D0E5697425","name":"Molecular Drug Targets","grant_number":"W1232-B24"},{"grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"name":"Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo and in vitro Models","grant_number":"715508","_id":"25444568-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}],"related_material":{"link":[{"relation":"press_release","description":"News on ISTA Website","url":"https://ista.ac.at/en/news/feed-them-or-lose-them/"}],"record":[{"id":"13107","relation":"dissertation_contains","status":"public"}]},"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"],"doi":"10.1016/j.cell.2023.02.037","keyword":["General Biochemistry","Genetics and Molecular Biology"],"language":[{"iso":"eng"}],"title":"Large neutral amino acid levels tune perinatal neuronal excitability and survival","citation":{"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>.","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.","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.","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>.","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.","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>","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>"},"ec_funded":1,"author":[{"id":"3B2ABCF4-F248-11E8-B48F-1D18A9856A87","full_name":"Knaus, Lisa","first_name":"Lisa","last_name":"Knaus"},{"id":"36035796-5ACA-11E9-A75E-7AF2E5697425","orcid":"0000-0003-1843-3173","full_name":"Basilico, Bernadette","first_name":"Bernadette","last_name":"Basilico"},{"last_name":"Malzl","first_name":"Daniel","full_name":"Malzl, Daniel"},{"first_name":"Maria","full_name":"Gerykova Bujalkova, Maria","last_name":"Gerykova Bujalkova"},{"last_name":"Smogavec","first_name":"Mateja","full_name":"Smogavec, Mateja"},{"first_name":"Lena A.","full_name":"Schwarz, Lena A.","last_name":"Schwarz"},{"id":"f141a35d-15a9-11ec-9fb2-fef6becc7b6f","first_name":"Sarah","full_name":"Gorkiewicz, Sarah","last_name":"Gorkiewicz"},{"first_name":"Nicole","full_name":"Amberg, Nicole","last_name":"Amberg","orcid":"0000-0002-3183-8207","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87"},{"id":"48EA0138-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7462-0048","full_name":"Pauler, Florian","first_name":"Florian","last_name":"Pauler"},{"last_name":"Knittl-Frank","full_name":"Knittl-Frank, Christian","first_name":"Christian"},{"last_name":"Tassinari","first_name":"Marianna","full_name":"Tassinari, Marianna","id":"7af593f1-d44a-11ed-bf94-a3646a6bb35e"},{"last_name":"Maulide","first_name":"Nuno","full_name":"Maulide, Nuno"},{"last_name":"Rülicke","full_name":"Rülicke, Thomas","first_name":"Thomas"},{"last_name":"Menche","first_name":"Jörg","full_name":"Menche, Jörg"},{"last_name":"Hippenmeyer","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"id":"3E57A680-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7673-7178","last_name":"Novarino","full_name":"Novarino, Gaia","first_name":"Gaia"}],"type":"journal_article","day":"27","isi":1,"publisher":"Elsevier","status":"public","intvolume":"       186","publication":"Cell","department":[{"_id":"SiHi"},{"_id":"GaNo"}],"quality_controlled":"1","page":"1950-1967.e25","date_created":"2023-04-05T08:15:40Z","month":"04"},{"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.","project":[{"_id":"25D61E48-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Molecular Mechanisms of Cerebral Cortex Development","grant_number":"618444"},{"grant_number":"24812","name":"Molecular Mechanisms of Radial Neuronal Migration","_id":"2625A13E-B435-11E9-9278-68D0E5697425"}],"related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"12726"},{"status":"public","id":"14530","relation":"dissertation_contains"}]},"doi":"10.1093/oons/kvac009","ddc":["570"],"language":[{"iso":"eng"}],"title":"Tissue-wide effects override cell-intrinsic gene function in radial neuron migration","ec_funded":1,"citation":{"short":"A.H. Hansen, F. Pauler, M. Riedl, C. Streicher, A.-M. Heger, S. Laukoter, C.M. Sommer, A. Nicolas, B. Hof, L.H. Tsai, T. Rülicke, S. Hippenmeyer, Oxford Open Neuroscience 1 (2022).","apa":"Hansen, A. H., Pauler, F., Riedl, M., Streicher, C., Heger, A.-M., Laukoter, S., … Hippenmeyer, S. (2022). Tissue-wide effects override cell-intrinsic gene function in radial neuron migration. <i>Oxford Open Neuroscience</i>. Oxford Academic. <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 Academic, 2022.","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.","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 Academic, 2022. <a href=\"https://doi.org/10.1093/oons/kvac009\">https://doi.org/10.1093/oons/kvac009</a>.","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 Academic, 2022, doi:<a href=\"https://doi.org/10.1093/oons/kvac009\">10.1093/oons/kvac009</a>."},"type":"journal_article","author":[{"first_name":"Andi H","full_name":"Hansen, Andi H","last_name":"Hansen","id":"38853E16-F248-11E8-B48F-1D18A9856A87"},{"id":"48EA0138-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7462-0048","last_name":"Pauler","full_name":"Pauler, Florian","first_name":"Florian"},{"first_name":"Michael","full_name":"Riedl, Michael","last_name":"Riedl","id":"3BE60946-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4844-6311"},{"id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","full_name":"Streicher, Carmen","first_name":"Carmen","last_name":"Streicher"},{"last_name":"Heger","first_name":"Anna-Magdalena","full_name":"Heger, Anna-Magdalena","id":"4B76FFD2-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Susanne","full_name":"Laukoter, Susanne","last_name":"Laukoter","orcid":"0000-0002-7903-3010","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87"},{"id":"4DF26D8C-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-1216-9105","first_name":"Christoph M","full_name":"Sommer, Christoph M","last_name":"Sommer"},{"id":"2A103192-F248-11E8-B48F-1D18A9856A87","last_name":"Nicolas","first_name":"Armel","full_name":"Nicolas, Armel"},{"orcid":"0000-0003-2057-2754","id":"3A374330-F248-11E8-B48F-1D18A9856A87","full_name":"Hof, Björn","first_name":"Björn","last_name":"Hof"},{"full_name":"Tsai, Li Huei","first_name":"Li Huei","last_name":"Tsai"},{"last_name":"Rülicke","first_name":"Thomas","full_name":"Rülicke, Thomas"},{"last_name":"Hippenmeyer","first_name":"Simon","full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061"}],"day":"07","publisher":"Oxford Academic","intvolume":"         1","status":"public","department":[{"_id":"SiHi"},{"_id":"BjHo"},{"_id":"LifeSc"},{"_id":"EM-Fac"}],"quality_controlled":"1","publication":"Oxford Open Neuroscience","date_created":"2022-02-25T07:52:11Z","month":"07","publication_identifier":{"eissn":["2753-149X"]},"acknowledged_ssus":[{"_id":"LifeSc"},{"_id":"PreCl"},{"_id":"Bio"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2023-11-30T10:55:12Z","has_accepted_license":"1","year":"2022","oa_version":"Published Version","article_type":"original","oa":1,"publication_status":"published","volume":1,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"file_date_updated":"2023-08-16T08:00:30Z","issue":"1","article_processing_charge":"No","_id":"10791","date_published":"2022-07-07T00:00:00Z","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"}],"article_number":"kvac009","file":[{"success":1,"date_created":"2023-08-16T08:00:30Z","content_type":"application/pdf","relation":"main_file","file_id":"14061","date_updated":"2023-08-16T08:00:30Z","access_level":"open_access","checksum":"822e76e056c07099d1fb27d1ece5941b","file_name":"2023_OxfordOpenNeuroscience_Hansen.pdf","file_size":4846551,"creator":"dernst"}]},{"pmid":1,"doi":"10.21203/rs.3.rs-1316167/v1","publication_identifier":{"eissn":["2693-5015"]},"date_updated":"2023-10-17T13:06:52Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","language":[{"iso":"eng"}],"external_id":{"pmid":["PPR454733"]},"title":"WDFY3 cell autonomously controls neuronal migration","citation":{"ama":"Schaaf Z, Tat L, Cannizzaro N, et al. WDFY3 cell autonomously controls neuronal migration. doi:<a href=\"https://doi.org/10.21203/rs.3.rs-1316167/v1\">10.21203/rs.3.rs-1316167/v1</a>","apa":"Schaaf, Z., Tat, L., Cannizzaro, N., Green, R., Rülicke, T., Hippenmeyer, S., &#38; Zarbalis, K. (n.d.). WDFY3 cell autonomously controls neuronal migration. Research Square. <a href=\"https://doi.org/10.21203/rs.3.rs-1316167/v1\">https://doi.org/10.21203/rs.3.rs-1316167/v1</a>","short":"Z. Schaaf, L. Tat, N. Cannizzaro, R. Green, T. Rülicke, S. Hippenmeyer, K. Zarbalis, (n.d.).","mla":"Schaaf, Zachary, et al. <i>WDFY3 Cell Autonomously Controls Neuronal Migration</i>. Research Square, doi:<a href=\"https://doi.org/10.21203/rs.3.rs-1316167/v1\">10.21203/rs.3.rs-1316167/v1</a>.","chicago":"Schaaf, Zachary, Lyvin Tat, Noemi Cannizzaro, Ralph Green, Thomas Rülicke, Simon Hippenmeyer, and K Zarbalis. “WDFY3 Cell Autonomously Controls Neuronal Migration.” Research Square, n.d. <a href=\"https://doi.org/10.21203/rs.3.rs-1316167/v1\">https://doi.org/10.21203/rs.3.rs-1316167/v1</a>.","ieee":"Z. Schaaf <i>et al.</i>, “WDFY3 cell autonomously controls neuronal migration.” Research Square.","ista":"Schaaf Z, Tat L, Cannizzaro N, Green R, Rülicke T, Hippenmeyer S, Zarbalis K. WDFY3 cell autonomously controls neuronal migration. <a href=\"https://doi.org/10.21203/rs.3.rs-1316167/v1\">10.21203/rs.3.rs-1316167/v1</a>."},"oa_version":"Preprint","year":"2022","type":"preprint","author":[{"last_name":"Schaaf","first_name":"Zachary","full_name":"Schaaf, Zachary"},{"first_name":"Lyvin","full_name":"Tat, Lyvin","last_name":"Tat"},{"last_name":"Cannizzaro","first_name":"Noemi","full_name":"Cannizzaro, Noemi"},{"first_name":"Ralph","full_name":"Green, Ralph","last_name":"Green"},{"first_name":"Thomas","full_name":"Rülicke, Thomas","last_name":"Rülicke"},{"last_name":"Hippenmeyer","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Zarbalis","first_name":"K","full_name":"Zarbalis, K"}],"day":"16","main_file_link":[{"url":"https://doi.org/10.21203/rs.3.rs-1316167/v1","open_access":"1"}],"oa":1,"publication_status":"submitted","publisher":"Research Square","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"department":[{"_id":"SiHi"}],"article_processing_charge":"No","page":"30","date_published":"2022-02-16T00:00:00Z","_id":"10792","date_created":"2022-02-25T07:53:26Z","abstract":[{"text":"Background\r\nProper cerebral cortical development depends on the tightly orchestrated migration of newly born neurons from the inner ventricular and subventricular zones to the outer cortical plate. Any disturbance in this process during prenatal stages may lead to neuronal migration disorders (NMDs), which can vary in extent from focal to global. Furthermore, NMDs show a substantial comorbidity with other neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous work demonstrated focal neuronal migration defects in mice carrying loss-of-function alleles of the recognized autism risk gene WDFY3. However, the cellular origins of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide critical insight into WDFY3-dependent disease pathology .\r\nMethods\r\nHere, in an effort to untangle the origins of NMDs in Wdfy3lacZ mice, we employed mosaic analysis with double markers (MADM). MADM technology enabled us to genetically distinctly track and phenotypically analyze mutant and wild type cells concomitantly in vivo using immunofluorescent techniques.\r\nResults\r\nWe revealed a cell autonomous requirement of WDFY3 for accurate laminar positioning of cortical projection neurons and elimination of mispositioned cells during early postnatal life. In addition, we identified significant deviations in dendritic arborization, as well as synaptic density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant neurons in Wdfy3-MADM reporter mice at postnatal stages. Limitations While Wdfy3 mutant mice have provided valuable insight into prenatal aspects of ASD pathology that remain inaccessible to investigation in humans, like most animal models, they do not a perfectly replicate all aspects of human ASD biology. The lack of human data makes it indeterminate whether morphological deviations described here apply to ASD patients.\r\nConclusions\r\nOur genetic approach revealed several cell autonomous requirements of Wdfy3 in neuronal development that could underly the pathogenic mechanisms of WDFY3-related ASD conditions. The results are also consistent with findings in other ASD animal models and patients and suggest an important role for Wdfy3 in regulating neuronal function and interconnectivity in postnatal life.","lang":"eng"}],"month":"02"},{"citation":{"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>.","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>.","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.","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>","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>","short":"N. Amberg, F. Pauler, C. Streicher, S. Hippenmeyer, Science Advances 8 (2022)."},"ec_funded":1,"title":"Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression","day":"01","author":[{"orcid":"0000-0002-3183-8207","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","first_name":"Nicole","full_name":"Amberg, Nicole","last_name":"Amberg"},{"id":"48EA0138-F248-11E8-B48F-1D18A9856A87","last_name":"Pauler","first_name":"Florian","full_name":"Pauler, Florian"},{"id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","full_name":"Streicher, Carmen","first_name":"Carmen","last_name":"Streicher"},{"last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","first_name":"Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87"}],"type":"journal_article","related_material":{"link":[{"url":"https://ista.ac.at/en/news/whole-tissue-shapes-brain-development/","description":"News on ISTA website","relation":"press_release"}]},"project":[{"grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"name":"Role of Eed in neural stem cell lineage progression","grant_number":"T0101031","call_identifier":"FWF","_id":"268F8446-B435-11E9-9278-68D0E5697425"}],"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.","language":[{"iso":"eng"}],"doi":"10.1126/sciadv.abq1263","ddc":["570"],"month":"11","date_created":"2022-04-26T15:04:50Z","publisher":"American Association for the Advancement of Science","publication":"Science Advances","department":[{"_id":"SiHi"}],"quality_controlled":"1","status":"public","intvolume":"         8","article_type":"original","year":"2022","oa_version":"Published Version","has_accepted_license":"1","scopus_import":"1","date_updated":"2023-05-31T12:24:10Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["2375-2548"]},"acknowledged_ssus":[{"_id":"PreCl"},{"_id":"Bio"},{"_id":"LifeSc"}],"article_processing_charge":"No","issue":"44","article_number":"abq1263","file":[{"creator":"patrickd","file_size":2973998,"file_name":"sciadv.abq1263.pdf","checksum":"0117023e188542082ca6693cf39e7f03","access_level":"open_access","date_updated":"2023-03-21T14:18:10Z","relation":"main_file","file_id":"12742","content_type":"application/pdf","date_created":"2023-03-21T14:18:10Z","success":1}],"date_published":"2022-11-01T00:00:00Z","_id":"11336","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"}],"publication_status":"published","oa":1,"file_date_updated":"2023-03-21T14:18:10Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"volume":8},{"publication_identifier":{"issn":["2405-4712"],"eissn":["2405-4720"]},"external_id":{"pmid":["35452605"],"isi":["000814124400002"]},"scopus_import":"1","date_updated":"2023-08-03T07:19:43Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","year":"2022","oa_version":"Published Version","article_type":"original","volume":13,"oa":1,"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.cels.2022.03.006"}],"publication_status":"published","abstract":[{"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.","lang":"eng"}],"_id":"11449","date_published":"2022-06-15T00:00:00Z","article_processing_charge":"No","issue":"6","doi":"10.1016/j.cels.2022.03.006","language":[{"iso":"eng"}],"pmid":1,"project":[{"call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"},{"_id":"25D92700-B435-11E9-9278-68D0E5697425","grant_number":"LS13-002","name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain"}],"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.","type":"journal_article","author":[{"last_name":"Anderson","full_name":"Anderson, Donovan J.","first_name":"Donovan J."},{"last_name":"Pauler","first_name":"Florian","full_name":"Pauler, Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Mckenna","full_name":"Mckenna, Aaron","first_name":"Aaron"},{"first_name":"Jay","full_name":"Shendure, Jay","last_name":"Shendure"},{"first_name":"Simon","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061"},{"full_name":"Horwitz, Marshall S.","first_name":"Marshall S.","last_name":"Horwitz"}],"day":"15","title":"Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development","citation":{"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>.","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.","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.","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>.","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>","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>","short":"D.J. Anderson, F. Pauler, A. Mckenna, J. Shendure, S. Hippenmeyer, M.S. Horwitz, Cell Systems 13 (2022) 438–453.e5."},"ec_funded":1,"status":"public","intvolume":"        13","publication":"Cell Systems","quality_controlled":"1","department":[{"_id":"SiHi"}],"isi":1,"publisher":"Elsevier","date_created":"2022-06-19T22:01:57Z","month":"06","page":"438-453.e5"},{"article_type":"original","year":"2022","oa_version":"Published Version","has_accepted_license":"1","external_id":{"isi":["000814641400001"]},"date_updated":"2023-08-03T07:21:32Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","publication_identifier":{"issn":["2040-2392"]},"article_number":"27","file":[{"relation":"main_file","file_id":"11461","content_type":"application/pdf","success":1,"date_created":"2022-06-24T08:22:59Z","file_size":7552298,"creator":"dernst","file_name":"2022_MolecularAutism_Schaaf.pdf","access_level":"open_access","date_updated":"2022-06-24T08:22:59Z","checksum":"525d2618e855139089bbfc3e3d49d1b2"}],"_id":"11460","date_published":"2022-06-22T00:00:00Z","abstract":[{"text":"Background: Proper cerebral cortical development depends on the tightly orchestrated migration of newly born neurons from the inner ventricular and subventricular zones to the outer cortical plate. Any disturbance in this process during prenatal stages may lead to neuronal migration disorders (NMDs), which can vary in extent from focal to global. Furthermore, NMDs show a substantial comorbidity with other neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous work demonstrated focal neuronal migration defects in mice carrying loss-of-function alleles of the recognized autism risk gene WDFY3. However, the cellular origins of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide critical insight into WDFY3-dependent disease pathology.\r\nMethods: Here, in an effort to untangle the origins of NMDs in Wdfy3lacZ mice, we employed mosaic analysis with double markers (MADM). MADM technology enabled us to genetically distinctly track and phenotypically analyze mutant and wild-type cells concomitantly in vivo using immunofluorescent techniques.\r\nResults: We revealed a cell autonomous requirement of WDFY3 for accurate laminar positioning of cortical projection neurons and elimination of mispositioned cells during early postnatal life. In addition, we identified significant deviations in dendritic arborization, as well as synaptic density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant neurons in Wdfy3-MADM reporter mice at postnatal stages.\r\nLimitations: While Wdfy3 mutant mice have provided valuable insight into prenatal aspects of ASD pathology that remain inaccessible to investigation in humans, like most animal models, they do not a perfectly replicate all aspects of human ASD biology. The lack of human data makes it indeterminate whether morphological deviations described here apply to ASD patients or some of the other neurodevelopmental conditions associated with WDFY3 mutation.\r\nConclusions: Our genetic approach revealed several cell autonomous requirements of WDFY3 in neuronal development that could underlie the pathogenic mechanisms of WDFY3-related neurodevelopmental conditions. The results are also consistent with findings in other ASD animal models and patients and suggest an important role for WDFY3 in regulating neuronal function and interconnectivity in postnatal life.","lang":"eng"}],"article_processing_charge":"No","file_date_updated":"2022-06-24T08:22:59Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"volume":13,"publication_status":"published","oa":1,"day":"22","type":"journal_article","author":[{"first_name":"Zachary A.","full_name":"Schaaf, Zachary A.","last_name":"Schaaf"},{"last_name":"Tat","full_name":"Tat, Lyvin","first_name":"Lyvin"},{"last_name":"Cannizzaro","first_name":"Noemi","full_name":"Cannizzaro, Noemi"},{"full_name":"Green, Ralph","first_name":"Ralph","last_name":"Green"},{"last_name":"Rülicke","first_name":"Thomas","full_name":"Rülicke, Thomas"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","first_name":"Simon","full_name":"Hippenmeyer, Simon"},{"full_name":"Zarbalis, Konstantinos S.","first_name":"Konstantinos S.","last_name":"Zarbalis"}],"citation":{"mla":"Schaaf, Zachary A., et al. “WDFY3 Mutation Alters Laminar Position and Morphology of Cortical Neurons.” <i>Molecular Autism</i>, vol. 13, 27, Springer Nature, 2022, doi:<a href=\"https://doi.org/10.1186/s13229-022-00508-3\">10.1186/s13229-022-00508-3</a>.","ieee":"Z. A. Schaaf <i>et al.</i>, “WDFY3 mutation alters laminar position and morphology of cortical neurons,” <i>Molecular Autism</i>, vol. 13. Springer Nature, 2022.","ista":"Schaaf ZA, Tat L, Cannizzaro N, Green R, Rülicke T, Hippenmeyer S, Zarbalis KS. 2022. WDFY3 mutation alters laminar position and morphology of cortical neurons. Molecular Autism. 13, 27.","chicago":"Schaaf, Zachary A., Lyvin Tat, Noemi Cannizzaro, Ralph Green, Thomas Rülicke, Simon Hippenmeyer, and Konstantinos S. Zarbalis. “WDFY3 Mutation Alters Laminar Position and Morphology of Cortical Neurons.” <i>Molecular Autism</i>. Springer Nature, 2022. <a href=\"https://doi.org/10.1186/s13229-022-00508-3\">https://doi.org/10.1186/s13229-022-00508-3</a>.","apa":"Schaaf, Z. A., Tat, L., Cannizzaro, N., Green, R., Rülicke, T., Hippenmeyer, S., &#38; Zarbalis, K. S. (2022). WDFY3 mutation alters laminar position and morphology of cortical neurons. <i>Molecular Autism</i>. Springer Nature. <a href=\"https://doi.org/10.1186/s13229-022-00508-3\">https://doi.org/10.1186/s13229-022-00508-3</a>","ama":"Schaaf ZA, Tat L, Cannizzaro N, et al. WDFY3 mutation alters laminar position and morphology of cortical neurons. <i>Molecular Autism</i>. 2022;13. doi:<a href=\"https://doi.org/10.1186/s13229-022-00508-3\">10.1186/s13229-022-00508-3</a>","short":"Z.A. Schaaf, L. Tat, N. Cannizzaro, R. Green, T. Rülicke, S. Hippenmeyer, K.S. Zarbalis, Molecular Autism 13 (2022)."},"title":"WDFY3 mutation alters laminar position and morphology of cortical neurons","keyword":["Psychiatry and Mental health","Developmental Biology","Developmental Neuroscience","Molecular Biology"],"language":[{"iso":"eng"}],"doi":"10.1186/s13229-022-00508-3","ddc":["570"],"related_material":{"link":[{"relation":"erratum","url":"https://doi.org/10.1186/s13229-023-00539-4"}]},"acknowledgement":"This study was funded by NIMH R21MH115347 to KSZ. KSZ is further supported by Shriners Hospitals for Children.\r\nWe would like to thank Angelo Harlan de Crescenzo for early contributions to this project.","month":"06","date_created":"2022-06-23T14:28:55Z","publication":"Molecular Autism","department":[{"_id":"SiHi"}],"quality_controlled":"1","intvolume":"        13","status":"public","publisher":"Springer Nature","isi":1},{"article_type":"original","oa_version":"Published Version","year":"2022","has_accepted_license":"1","date_updated":"2023-08-02T06:53:07Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","external_id":{"isi":["000822975900002"]},"scopus_import":"1","acknowledged_ssus":[{"_id":"Bio"},{"_id":"EM-Fac"},{"_id":"PreCl"},{"_id":"LifeSc"}],"publication_identifier":{"eissn":["1529-2916"],"issn":["1529-2908"]},"file":[{"date_created":"2022-07-25T07:11:32Z","success":1,"file_id":"11642","relation":"main_file","content_type":"application/pdf","checksum":"628e7b49809f22c75b428842efe70c68","access_level":"open_access","date_updated":"2022-07-25T07:11:32Z","creator":"dernst","file_size":11475325,"file_name":"2022_NatureImmunology_Assen.pdf"}],"_id":"9794","date_published":"2022-07-11T00:00:00Z","abstract":[{"lang":"eng","text":"Lymph nodes (LNs) comprise two main structural elements: fibroblastic reticular cells that form dedicated niches for immune cell interaction and capsular fibroblasts that build a shell around the organ. Immunological challenge causes LNs to increase more than tenfold in size within a few days. Here, we characterized the biomechanics of LN swelling on the cellular and organ scale. We identified lymphocyte trapping by influx and proliferation as drivers of an outward pressure force, causing fibroblastic reticular cells of the T-zone (TRCs) and their associated conduits to stretch. After an initial phase of relaxation, TRCs sensed the resulting strain through cell matrix adhesions, which coordinated local growth and remodeling of the stromal network. While the expanded TRC network readopted its typical configuration, a massive fibrotic reaction of the organ capsule set in and countered further organ expansion. Thus, different fibroblast populations mechanically control LN swelling in a multitier fashion."}],"article_processing_charge":"No","file_date_updated":"2022-07-25T07:11:32Z","volume":23,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"publication_status":"published","oa":1,"day":"11","type":"journal_article","author":[{"id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-3470-6119","last_name":"Assen","first_name":"Frank P","full_name":"Assen, Frank P"},{"last_name":"Abe","full_name":"Abe, Jun","first_name":"Jun"},{"id":"4167FE56-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6625-3348","last_name":"Hons","full_name":"Hons, Miroslav","first_name":"Miroslav"},{"orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","full_name":"Hauschild, Robert","first_name":"Robert","last_name":"Hauschild"},{"id":"40B34FE2-F248-11E8-B48F-1D18A9856A87","last_name":"Shamipour","first_name":"Shayan","full_name":"Shamipour, Shayan"},{"id":"3F99E422-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9735-5315","full_name":"Kaufmann, Walter","first_name":"Walter","last_name":"Kaufmann"},{"last_name":"Costanzo","first_name":"Tommaso","full_name":"Costanzo, Tommaso","id":"D93824F4-D9BA-11E9-BB12-F207E6697425","orcid":"0000-0001-9732-3815"},{"first_name":"Gabriel","full_name":"Krens, Gabriel","last_name":"Krens","orcid":"0000-0003-4761-5996","id":"2B819732-F248-11E8-B48F-1D18A9856A87"},{"id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","full_name":"Brown, Markus","first_name":"Markus","last_name":"Brown"},{"last_name":"Ludewig","full_name":"Ludewig, Burkhard","first_name":"Burkhard"},{"last_name":"Hippenmeyer","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"id":"39427864-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0912-4566","first_name":"Carl-Philipp J","full_name":"Heisenberg, Carl-Philipp J","last_name":"Heisenberg"},{"last_name":"Weninger","full_name":"Weninger, Wolfgang","first_name":"Wolfgang"},{"id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6005-1561","first_name":"Edouard B","full_name":"Hannezo, Edouard B","last_name":"Hannezo"},{"first_name":"Sanjiv A.","full_name":"Luther, Sanjiv A.","last_name":"Luther"},{"last_name":"Stein","full_name":"Stein, Jens V.","first_name":"Jens V."},{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","orcid":"0000-0002-4561-241X","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"ec_funded":1,"citation":{"short":"F.P. Assen, J. Abe, M. Hons, R. Hauschild, S. Shamipour, W. Kaufmann, T. Costanzo, G. Krens, M. Brown, B. Ludewig, S. Hippenmeyer, C.-P.J. Heisenberg, W. Weninger, E.B. Hannezo, S.A. Luther, J.V. Stein, M.K. Sixt, Nature Immunology 23 (2022) 1246–1255.","apa":"Assen, F. P., Abe, J., Hons, M., Hauschild, R., Shamipour, S., Kaufmann, W., … Sixt, M. K. (2022). Multitier mechanics control stromal adaptations in swelling lymph nodes. <i>Nature Immunology</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41590-022-01257-4\">https://doi.org/10.1038/s41590-022-01257-4</a>","ama":"Assen FP, Abe J, Hons M, et al. Multitier mechanics control stromal adaptations in swelling lymph nodes. <i>Nature Immunology</i>. 2022;23:1246-1255. doi:<a href=\"https://doi.org/10.1038/s41590-022-01257-4\">10.1038/s41590-022-01257-4</a>","ista":"Assen FP, Abe J, Hons M, Hauschild R, Shamipour S, Kaufmann W, Costanzo T, Krens G, Brown M, Ludewig B, Hippenmeyer S, Heisenberg C-PJ, Weninger W, Hannezo EB, Luther SA, Stein JV, Sixt MK. 2022. Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. 23, 1246–1255.","ieee":"F. P. Assen <i>et al.</i>, “Multitier mechanics control stromal adaptations in swelling lymph nodes,” <i>Nature Immunology</i>, vol. 23. Springer Nature, pp. 1246–1255, 2022.","chicago":"Assen, Frank P, Jun Abe, Miroslav Hons, Robert Hauschild, Shayan Shamipour, Walter Kaufmann, Tommaso Costanzo, et al. “Multitier Mechanics Control Stromal Adaptations in Swelling Lymph Nodes.” <i>Nature Immunology</i>. Springer Nature, 2022. <a href=\"https://doi.org/10.1038/s41590-022-01257-4\">https://doi.org/10.1038/s41590-022-01257-4</a>.","mla":"Assen, Frank P., et al. “Multitier Mechanics Control Stromal Adaptations in Swelling Lymph Nodes.” <i>Nature Immunology</i>, vol. 23, Springer Nature, 2022, pp. 1246–55, doi:<a href=\"https://doi.org/10.1038/s41590-022-01257-4\">10.1038/s41590-022-01257-4</a>."},"title":"Multitier mechanics control stromal adaptations in swelling lymph nodes","language":[{"iso":"eng"}],"doi":"10.1038/s41590-022-01257-4","ddc":["570"],"acknowledgement":"This research was supported by the Scientific Service Units of IST Austria through resources provided by the Imaging and Optics, Electron Microscopy, Preclinical and Life Science Facilities. We thank C. Moussion for providing anti-PNAd antibody and D. Critchley for Talin1-floxed mice, and E. Papusheva for providing a custom 3D channel alignment script. This work was supported by a European Research Council grant ERC-CoG-72437 to M.S. M.H. was supported by Czech Sciencundation GACR 20-24603Y and Charles University PRIMUS/20/MED/013.","project":[{"call_identifier":"H2020","_id":"25FE9508-B435-11E9-9278-68D0E5697425","grant_number":"724373","name":"Cellular navigation along spatial gradients"}],"month":"07","date_created":"2021-08-06T09:09:11Z","page":"1246-1255","department":[{"_id":"SiHi"},{"_id":"CaHe"},{"_id":"EdHa"},{"_id":"EM-Fac"},{"_id":"Bio"},{"_id":"MiSi"}],"quality_controlled":"1","publication":"Nature Immunology","intvolume":"        23","status":"public","publisher":"Springer Nature","isi":1},{"_id":"8544","abstract":[{"lang":"eng","text":"The synaptotrophic hypothesis posits that synapse formation stabilizes dendritic branches, yet this hypothesis has not been causally tested in vivo in the mammalian brain. Presynaptic ligand cerebellin-1 (Cbln1) and postsynaptic receptor GluD2 mediate synaptogenesis between granule cells and Purkinje cells in the molecular layer of the cerebellar cortex. Here we show that sparse but not global knockout of GluD2 causes under-elaboration of Purkinje cell dendrites in the deep molecular layer and overelaboration in the superficial molecular layer. Developmental, overexpression, structure-function, and genetic epistasis analyses indicate that dendrite morphogenesis defects result from competitive synaptogenesis in a Cbln1/GluD2-dependent manner. A generative model of dendritic growth based on competitive synaptogenesis largely recapitulates GluD2 sparse and global knockout phenotypes. Our results support the synaptotrophic hypothesis at initial stages of dendrite development, suggest a second mode in which cumulative synapse formation inhibits further dendrite growth, and highlight the importance of competition in dendrite morphogenesis."}],"date_published":"2021-02-17T00:00:00Z","issue":"4","article_processing_charge":"No","volume":109,"publication_status":"published","oa":1,"main_file_link":[{"url":"https://doi.org/10.1101/2020.06.14.151258","open_access":"1"}],"article_type":"original","oa_version":"Preprint","year":"2021","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2024-03-06T12:12:48Z","scopus_import":"1","publication_identifier":{"eissn":["1097-4199"]},"month":"02","date_created":"2020-09-21T11:59:47Z","page":"P629-644.E8","department":[{"_id":"SiHi"}],"quality_controlled":"1","publication":"Neuron","intvolume":"       109","status":"public","publisher":"Elsevier","day":"17","author":[{"last_name":"Takeo","full_name":"Takeo, Yukari H.","first_name":"Yukari H."},{"last_name":"Shuster","full_name":"Shuster, S. Andrew","first_name":"S. Andrew"},{"last_name":"Jiang","first_name":"Linnie","full_name":"Jiang, Linnie"},{"last_name":"Hu","full_name":"Hu, Miley","first_name":"Miley"},{"last_name":"Luginbuhl","full_name":"Luginbuhl, David J.","first_name":"David J."},{"full_name":"Rülicke, Thomas","first_name":"Thomas","last_name":"Rülicke"},{"id":"475990FE-F248-11E8-B48F-1D18A9856A87","last_name":"Contreras","first_name":"Ximena","full_name":"Contreras, Ximena"},{"last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061"},{"first_name":"Mark J.","full_name":"Wagner, Mark J.","last_name":"Wagner"},{"full_name":"Ganguli, Surya","first_name":"Surya","last_name":"Ganguli"},{"last_name":"Luo","full_name":"Luo, Liqun","first_name":"Liqun"}],"type":"journal_article","ec_funded":1,"citation":{"apa":"Takeo, Y. H., Shuster, S. A., Jiang, L., Hu, M., Luginbuhl, D. J., Rülicke, T., … Luo, L. (2021). GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2020.11.028\">https://doi.org/10.1016/j.neuron.2020.11.028</a>","ama":"Takeo YH, Shuster SA, Jiang L, et al. GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. <i>Neuron</i>. 2021;109(4):P629-644.E8. doi:<a href=\"https://doi.org/10.1016/j.neuron.2020.11.028\">10.1016/j.neuron.2020.11.028</a>","short":"Y.H. Takeo, S.A. Shuster, L. Jiang, M. Hu, D.J. Luginbuhl, T. Rülicke, X. Contreras, S. Hippenmeyer, M.J. Wagner, S. Ganguli, L. Luo, Neuron 109 (2021) P629–644.E8.","mla":"Takeo, Yukari H., et al. “GluD2- and Cbln1-Mediated Competitive Synaptogenesis Shapes the Dendritic Arbors of Cerebellar Purkinje Cells.” <i>Neuron</i>, vol. 109, no. 4, Elsevier, 2021, p. P629–644.E8, doi:<a href=\"https://doi.org/10.1016/j.neuron.2020.11.028\">10.1016/j.neuron.2020.11.028</a>.","ista":"Takeo YH, Shuster SA, Jiang L, Hu M, Luginbuhl DJ, Rülicke T, Contreras X, Hippenmeyer S, Wagner MJ, Ganguli S, Luo L. 2021. GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. Neuron. 109(4), P629–644.E8.","ieee":"Y. H. Takeo <i>et al.</i>, “GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells,” <i>Neuron</i>, vol. 109, no. 4. Elsevier, p. P629–644.E8, 2021.","chicago":"Takeo, Yukari H., S. Andrew Shuster, Linnie Jiang, Miley Hu, David J. Luginbuhl, Thomas Rülicke, Ximena Contreras, et al. “GluD2- and Cbln1-Mediated Competitive Synaptogenesis Shapes the Dendritic Arbors of Cerebellar Purkinje Cells.” <i>Neuron</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.neuron.2020.11.028\">https://doi.org/10.1016/j.neuron.2020.11.028</a>."},"title":"GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells","language":[{"iso":"eng"}],"doi":"10.1016/j.neuron.2020.11.028","acknowledgement":"We thank M. Mishina for GluD2fl frozen embryos, T.C. Südhof and J.I. Morgan for Cbln1fl mice, L. Anderson for help in generating the MADM alleles, W. Joo for a previously unpublished construct, M. Yuzaki, K. Shen, J. Ding, and members of the Luo lab, including J.M. Kebschull, H. Li, J. Li, T. Li, C.M. McLaughlin, D. Pederick, J. Ren, D.C. Wang and C. Xu for discussions and critiques of the manuscript, and M. Yuzaki for supporting Y.H.T. during the final phase of this project. Y.H.T. was supported by a JSPS fellowship; S.A.S. was supported by a Stanford Graduate Fellowship and an NSF Predoctoral Fellowship; L.J. is supported by a Stanford Graduate Fellowship and an NSF Predoctoral Fellowship; M.J.W. is supported by a Burroughs Wellcome Fund CASI Award. This work was supported by an NIH grant (R01-NS050538) to L.L.; the European Research Council (ERC) under the European Union's Horizon 2020 research and innovations programme (No. 725780 LinPro) to S.H.; and Simons and James S. McDonnell Foundations and an NSF CAREER award to S.G.; L.L. is an HHMI investigator.","project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780","_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}]},{"acknowledgement":"This work was supported by the program “Investissements d’avenir” ANR-10-IAIHU-06 , ICM , a Sorbonne Université Emergence grant, an Allen Distinguished Investigator Award , and the Roger De Spoelberch Foundation Prize (to B.A.H.); Armenise-Harvard Foundation , AIRC , and CARITRO (to L.T.); and the European Research Council under the European Union’s Horizon 2020 research and innovation programme grant agreement no. 725780 LinPro (to S.H.). T.Z. and T.L. were supported by doctoral fellowships from the China Scholarship Council and A.H.H. by a doctoral DOC fellowship of the Austrian Academy of Sciences ( 24812 ). All animal work was conducted at the PHENO-ICMice facility. The Core is supported by 2 “Investissements d’avenir” (ANR-10- IAIHU-06 and ANR-11-INBS-0011-NeurATRIS) and the “Fondation pour la Recherche Médicale.” Light microscopy work was carried out at ICM’s imaging core facility, ICM.Quant, and analysis of scRNA-seq data was carried out at ICM’s bioinformatics core facility, iCONICS. We thank Paulina Ejsmont, Natalia Danda, and Nathalie De Geest for technical support. We are grateful to Dr. Shahragim TAJBAKHSH for providing R26Rstop-NICD-nGFP transgenic mice, Dr. Bart De Strooper for Psn1-deficient mice, Dr. Jean-Christophe Marine for Gt(ROSA)26SortdTom reporter mice, and Dr. Martinez Barbera for Sox2CreERT2 mice. We also give thanks to Dr. Mikio Hoshino for providing Atoh1 and Ptf1a antibodies. B.A.H. is an Einstein Visiting Fellow of the Berlin Institute of Health .","project":[{"call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780"},{"_id":"2625A13E-B435-11E9-9278-68D0E5697425","grant_number":"24812","name":"Molecular Mechanisms of Radial Neuronal Migration"}],"pmid":1,"related_material":{"link":[{"relation":"earlier_version","url":"https://doi.org/10.1101/2020.03.18.997205"}]},"language":[{"iso":"eng"}],"ddc":["570"],"doi":"10.1016/j.celrep.2021.109208","ec_funded":1,"citation":{"short":"T. Zhang, T. Liu, N. Mora, J. Guegan, M. Bertrand, X. Contreras, A.H. Hansen, C. Streicher, M. Anderle, N. Danda, L. Tiberi, S. Hippenmeyer, B.A. Hassan, Cell Reports 35 (2021).","ama":"Zhang T, Liu T, Mora N, et al. Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum. <i>Cell Reports</i>. 2021;35(10). doi:<a href=\"https://doi.org/10.1016/j.celrep.2021.109208\">10.1016/j.celrep.2021.109208</a>","apa":"Zhang, T., Liu, T., Mora, N., Guegan, J., Bertrand, M., Contreras, X., … Hassan, B. A. (2021). Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum. <i>Cell Reports</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.celrep.2021.109208\">https://doi.org/10.1016/j.celrep.2021.109208</a>","chicago":"Zhang, Tingting, Tengyuan Liu, Natalia Mora, Justine Guegan, Mathilde Bertrand, Ximena Contreras, Andi H Hansen, et al. “Generation of Excitatory and Inhibitory Neurons from Common Progenitors via Notch Signaling in the Cerebellum.” <i>Cell Reports</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.celrep.2021.109208\">https://doi.org/10.1016/j.celrep.2021.109208</a>.","ieee":"T. Zhang <i>et al.</i>, “Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum,” <i>Cell Reports</i>, vol. 35, no. 10. Elsevier, 2021.","ista":"Zhang T, Liu T, Mora N, Guegan J, Bertrand M, Contreras X, Hansen AH, Streicher C, Anderle M, Danda N, Tiberi L, Hippenmeyer S, Hassan BA. 2021. Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum. Cell Reports. 35(10), 109208.","mla":"Zhang, Tingting, et al. “Generation of Excitatory and Inhibitory Neurons from Common Progenitors via Notch Signaling in the Cerebellum.” <i>Cell Reports</i>, vol. 35, no. 10, 109208, Elsevier, 2021, doi:<a href=\"https://doi.org/10.1016/j.celrep.2021.109208\">10.1016/j.celrep.2021.109208</a>."},"title":"Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum","day":"08","type":"journal_article","author":[{"last_name":"Zhang","first_name":"Tingting","full_name":"Zhang, Tingting"},{"full_name":"Liu, Tengyuan","first_name":"Tengyuan","last_name":"Liu"},{"last_name":"Mora","first_name":"Natalia","full_name":"Mora, Natalia"},{"full_name":"Guegan, Justine","first_name":"Justine","last_name":"Guegan"},{"first_name":"Mathilde","full_name":"Bertrand, Mathilde","last_name":"Bertrand"},{"id":"475990FE-F248-11E8-B48F-1D18A9856A87","full_name":"Contreras, Ximena","first_name":"Ximena","last_name":"Contreras"},{"first_name":"Andi H","full_name":"Hansen, Andi H","last_name":"Hansen","id":"38853E16-F248-11E8-B48F-1D18A9856A87"},{"id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","last_name":"Streicher","full_name":"Streicher, Carmen","first_name":"Carmen"},{"last_name":"Anderle","full_name":"Anderle, Marica","first_name":"Marica"},{"last_name":"Danda","full_name":"Danda, Natasha","first_name":"Natasha"},{"full_name":"Tiberi, Luca","first_name":"Luca","last_name":"Tiberi"},{"orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer"},{"first_name":"Bassem A.","full_name":"Hassan, Bassem A.","last_name":"Hassan"}],"publisher":"Elsevier","isi":1,"quality_controlled":"1","department":[{"_id":"SiHi"}],"publication":"Cell Reports","intvolume":"        35","status":"public","month":"06","date_created":"2020-09-21T12:00:48Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","date_updated":"2023-08-04T11:00:48Z","scopus_import":"1","external_id":{"isi":["000659894300001"],"pmid":["34107249 "]},"publication_identifier":{"eissn":[" 22111247"]},"article_type":"original","year":"2021","has_accepted_license":"1","oa_version":"Published Version","publication_status":"published","oa":1,"file_date_updated":"2021-06-15T14:01:35Z","volume":35,"tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","image":"/images/cc_by_nc_nd.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)"},"issue":"10","article_processing_charge":"No","file":[{"success":1,"date_created":"2021-06-15T14:01:35Z","content_type":"application/pdf","relation":"main_file","file_id":"9554","date_updated":"2021-06-15T14:01:35Z","access_level":"open_access","checksum":"7def3d42ebc8f5675efb6f38819e3e2e","file_name":"2021_CellReports_Zhang.pdf","file_size":8900385,"creator":"cziletti"}],"article_number":"109208","date_published":"2021-06-08T00:00:00Z","_id":"8546","abstract":[{"lang":"eng","text":"Brain neurons arise from relatively few progenitors generating an enormous diversity of neuronal types. Nonetheless, a cardinal feature of mammalian brain neurogenesis is thought to be that excitatory and inhibitory neurons derive from separate, spatially segregated progenitors. Whether bi-potential progenitors with an intrinsic capacity to generate both lineages exist and how such a fate decision may be regulated are unknown. Using cerebellar development as a model, we discover that individual progenitors can give rise to both inhibitory and excitatory lineages. Gradations of Notch activity determine the fates of the progenitors and their daughters. Daughters with the highest levels of Notch activity retain the progenitor fate, while intermediate levels of Notch activity generate inhibitory neurons, and daughters with very low levels of Notch signaling adopt the excitatory fate. Therefore, Notch-mediated binary cell fate choice is a mechanism for regulating the ratio of excitatory to inhibitory neurons from common progenitors."}]},{"type":"journal_article","author":[{"last_name":"Hanganu-Opatz","first_name":"Ileana L.","full_name":"Hanganu-Opatz, Ileana L."},{"last_name":"Butt","full_name":"Butt, Simon J. B.","first_name":"Simon J. B."},{"orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","first_name":"Simon","last_name":"Hippenmeyer"},{"full_name":"De Marco García, Natalia V.","first_name":"Natalia V.","last_name":"De Marco García"},{"last_name":"Cardin","first_name":"Jessica A.","full_name":"Cardin, Jessica A."},{"first_name":"Bradley","full_name":"Voytek, Bradley","last_name":"Voytek"},{"last_name":"Muotri","first_name":"Alysson R.","full_name":"Muotri, Alysson R."}],"day":"03","title":"The logic of developing neocortical circuits in health and disease","citation":{"ama":"Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, et al. The logic of developing neocortical circuits in health and disease. <i>The Journal of Neuroscience</i>. 2021;41(5):813-822. doi:<a href=\"https://doi.org/10.1523/jneurosci.1655-20.2020\">10.1523/jneurosci.1655-20.2020</a>","apa":"Hanganu-Opatz, I. L., Butt, S. J. B., Hippenmeyer, S., De Marco García, N. V., Cardin, J. A., Voytek, B., &#38; Muotri, A. R. (2021). The logic of developing neocortical circuits in health and disease. <i>The Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/jneurosci.1655-20.2020\">https://doi.org/10.1523/jneurosci.1655-20.2020</a>","short":"I.L. Hanganu-Opatz, S.J.B. Butt, S. Hippenmeyer, N.V. De Marco García, J.A. Cardin, B. Voytek, A.R. Muotri, The Journal of Neuroscience 41 (2021) 813–822.","mla":"Hanganu-Opatz, Ileana L., et al. “The Logic of Developing Neocortical Circuits in Health and Disease.” <i>The Journal of Neuroscience</i>, vol. 41, no. 5, Society for Neuroscience, 2021, pp. 813–22, doi:<a href=\"https://doi.org/10.1523/jneurosci.1655-20.2020\">10.1523/jneurosci.1655-20.2020</a>.","chicago":"Hanganu-Opatz, Ileana L., Simon J. B. Butt, Simon Hippenmeyer, Natalia V. De Marco García, Jessica A. Cardin, Bradley Voytek, and Alysson R. Muotri. “The Logic of Developing Neocortical Circuits in Health and Disease.” <i>The Journal of Neuroscience</i>. Society for Neuroscience, 2021. <a href=\"https://doi.org/10.1523/jneurosci.1655-20.2020\">https://doi.org/10.1523/jneurosci.1655-20.2020</a>.","ista":"Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, De Marco García NV, Cardin JA, Voytek B, Muotri AR. 2021. The logic of developing neocortical circuits in health and disease. The Journal of Neuroscience. 41(5), 813–822.","ieee":"I. L. Hanganu-Opatz <i>et al.</i>, “The logic of developing neocortical circuits in health and disease,” <i>The Journal of Neuroscience</i>, vol. 41, no. 5. Society for Neuroscience, pp. 813–822, 2021."},"ec_funded":1,"doi":"10.1523/jneurosci.1655-20.2020","ddc":["570"],"keyword":["General Neuroscience"],"language":[{"iso":"eng"}],"project":[{"grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425"},{"name":"Molecular Mechanisms of Neural Stem Cell Lineage Progression","grant_number":"F07805","_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E"}],"pmid":1,"acknowledgement":"Work in the I.L.H.-O. laboratory was supported by European Research Council Grant ERC-2015-CoG 681577 and German Research Foundation Ha 4466/10-1, Ha4466/11-1, Ha4466/12-1, SPP 1665, and SFB 936B5. Work in the S.J.B.B. laboratory was supported by Biotechnology and Biological Sciences Research Council BB/P003796/1, Medical Research Council MR/K004387/1 and MR/T033320/1, Wellcome Trust 215199/Z/19/Z and 102386/Z/13/Z, and John Fell Fund. Work in the S.H. laboratory was supported by European Research Council Grants ERC-2016-CoG 725780 LinPro and FWF SFB F78. This work was supported by National Institutes of Health Grant NIMH 1R01MH110553 to N.V.D.M.G. Work in the J.A.C. laboratory was supported by the Ludwig Family Foundation, Simons Foundation SFARI Research Award, and National Institutes of Health/National Institute of Mental Health R01 MH102365 and R01MH113852. The B.V. laboratory was supported by Whitehall Foundation 2017-12-73, National Science Foundation 1736028, National Institutes of Health, National Institute of General Medical Sciences R01GM134363-01, and Halıcıoğlu Data Science Institute Fellowship. This work was supported by the University of California San Diego School of Medicine.","date_created":"2021-02-03T12:23:51Z","month":"02","page":"813-822","intvolume":"        41","status":"public","publication":"The Journal of Neuroscience","department":[{"_id":"SiHi"}],"quality_controlled":"1","isi":1,"publisher":"Society for Neuroscience","year":"2021","has_accepted_license":"1","oa_version":"Published Version","article_type":"original","publication_identifier":{"issn":["0270-6474"],"eissn":["1529-2401"]},"scopus_import":"1","external_id":{"pmid":["33431633"],"isi":["000616763400002"]},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","date_updated":"2023-09-05T14:03:17Z","_id":"9073","date_published":"2021-02-03T00:00:00Z","abstract":[{"lang":"eng","text":"The sensory and cognitive abilities of the mammalian neocortex are underpinned by intricate columnar and laminar circuits formed from an array of diverse neuronal populations. One approach to determining how interactions between these circuit components give rise to complex behavior is to investigate the rules by which cortical circuits are formed and acquire functionality during development. This review summarizes recent research on the development of the neocortex, from genetic determination in neural stem cells through to the dynamic role that specific neuronal populations play in the earliest circuits of neocortex, and how they contribute to emergent function and cognition. While many of these endeavors take advantage of model systems, consideration will also be given to advances in our understanding of activity in nascent human circuits. Such cross-species perspective is imperative when investigating the mechanisms underlying the dysfunction of early neocortical circuits in neurodevelopmental disorders, so that one can identify targets amenable to therapeutic intervention."}],"file":[{"checksum":"578fd7ed1a0aef74bce61bea2d987b33","date_updated":"2022-05-27T06:59:55Z","access_level":"open_access","file_name":"2021_JourNeuroscience_Hanganu.pdf","creator":"dernst","file_size":1031150,"date_created":"2022-05-27T06:59:55Z","success":1,"content_type":"application/pdf","relation":"main_file","file_id":"11414"}],"article_processing_charge":"No","issue":"5","volume":41,"file_date_updated":"2022-05-27T06:59:55Z","oa":1,"publication_status":"published"},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-02-04T07:29:53Z","language":[{"iso":"eng"}],"doi":"10.1101/2020.12.31.425016","project":[{"call_identifier":"H2020","_id":"260018B0-B435-11E9-9278-68D0E5697425","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","grant_number":"725780"}],"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.","day":"01","author":[{"last_name":"Anderson","first_name":"Donovan J.","full_name":"Anderson, Donovan J."},{"id":"48EA0138-F248-11E8-B48F-1D18A9856A87","last_name":"Pauler","full_name":"Pauler, Florian","first_name":"Florian"},{"first_name":"Aaron","full_name":"McKenna, Aaron","last_name":"McKenna"},{"last_name":"Shendure","full_name":"Shendure, Jay","first_name":"Jay"},{"last_name":"Hippenmeyer","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Horwitz, Marshall S.","first_name":"Marshall S.","last_name":"Horwitz"}],"type":"preprint","year":"2021","oa_version":"Preprint","citation":{"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.","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>.","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>.","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>.","short":"D.J. Anderson, F. Pauler, A. McKenna, J. Shendure, S. Hippenmeyer, M.S. Horwitz, BioRxiv (n.d.).","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>","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>"},"ec_funded":1,"title":"Simultaneous identification of brain cell type and lineage via single cell RNA sequencing","publication":"bioRxiv","department":[{"_id":"SiHi"}],"status":"public","publisher":"Cold Spring Harbor Laboratory","publication_status":"submitted","oa":1,"main_file_link":[{"url":"https://doi.org/10.1101/2020.12.31.425016","open_access":"1"}],"month":"01","abstract":[{"text":"Acquired mutations are sufficiently frequent such that the genome of a single cell offers a record of its history of cell divisions. Among more common somatic genomic alterations are loss of heterozygosity (LOH). Large LOH events are potentially detectable in single cell RNA sequencing (scRNA-seq) datasets as tracts of monoallelic expression for constitutionally heterozygous single nucleotide variants (SNVs) located among contiguous genes. We identified runs of monoallelic expression, consistent with LOH, uniquely distributed throughout the genome in single cell brain cortex transcriptomes of F1 hybrids involving different inbred mouse strains. We then phylogenetically reconstructed single cell lineages and simultaneously identified cell types by corresponding gene expression patterns. Our results are consistent with progenitor cells giving rise to multiple cortical cell types through stereotyped expansion and distinct waves of neurogenesis. Compared to engineered recording systems, LOH events accumulate throughout the genome and across the lifetime of an organism, affording tremendous capacity for encoding lineage information and increasing resolution for later cell divisions. This approach can conceivably be computationally incorporated into scRNA-seq analysis and may be useful for organisms where genetic engineering is prohibitive, such as humans.","lang":"eng"}],"_id":"9082","date_created":"2021-02-04T07:23:23Z","date_published":"2021-01-01T00:00:00Z","article_processing_charge":"No"},{"external_id":{"pmid":["33600873"],"isi":["000635575000005"]},"scopus_import":"1","date_updated":"2023-08-07T13:48:26Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","publication_identifier":{"issn":["0197-0186"]},"article_type":"original","has_accepted_license":"1","year":"2021","oa_version":"Published Version","publication_status":"published","oa":1,"file_date_updated":"2021-08-11T12:30:38Z","tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","image":"/images/cc_by_nc_nd.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)"},"volume":145,"article_processing_charge":"Yes (via OA deal)","issue":"5","article_number":"104986","file":[{"content_type":"application/pdf","file_id":"9883","relation":"main_file","date_created":"2021-08-11T12:30:38Z","success":1,"file_name":"2021_NCI_Pauler.pdf","creator":"kschuh","file_size":7083499,"checksum":"c6d7a40089cd29e289f9b22e75768304","date_updated":"2021-08-11T12:30:38Z","access_level":"open_access"}],"date_published":"2021-05-01T00:00:00Z","_id":"9188","abstract":[{"lang":"eng","text":"Genomic imprinting is an epigenetic mechanism that results in parental allele-specific expression of ~1% of all genes in mouse and human. Imprinted genes are key developmental regulators and play pivotal roles in many biological processes such as nutrient transfer from the mother to offspring and neuronal development. Imprinted genes are also involved in human disease, including neurodevelopmental disorders, and often occur in clusters that are regulated by a common imprint control region (ICR). In extra-embryonic tissues ICRs can act over large distances, with the largest surrounding Igf2r spanning over 10 million base-pairs. Besides classical imprinted expression that shows near exclusive maternal or paternal expression, widespread biased imprinted expression has been identified mainly in brain. In this review we discuss recent developments mapping cell type specific imprinted expression in extra-embryonic tissues and neocortex in the mouse. We highlight the advantages of using an inducible uniparental chromosome disomy (UPD) system to generate cells carrying either two maternal or two paternal copies of a specific chromosome to analyze the functional consequences of genomic imprinting. Mosaic Analysis with Double Markers (MADM) allows fluorescent labeling and concomitant induction of UPD sparsely in specific cell types, and thus to over-express or suppress all imprinted genes on that chromosome. To illustrate the utility of this technique, we explain how MADM-induced UPD revealed new insights about the function of the well-studied Cdkn1c imprinted gene, and how MADM-induced UPDs led to identification of highly cell type specific phenotypes related to perturbed imprinted expression in the mouse neocortex. Finally, we give an outlook on how MADM could be used to probe cell type specific imprinted expression in other tissues in mouse, particularly in extra-embryonic tissues."}],"pmid":1,"project":[{"_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"},{"_id":"25D92700-B435-11E9-9278-68D0E5697425","name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain","grant_number":"LS13-002"}],"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.","keyword":["Cell Biology","Cellular and Molecular Neuroscience"],"language":[{"iso":"eng"}],"ddc":["570"],"doi":"10.1016/j.neuint.2021.104986","citation":{"short":"F. Pauler, Q. Hudson, S. Laukoter, S. Hippenmeyer, Neurochemistry International 145 (2021).","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>","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.","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>.","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>."},"ec_funded":1,"title":"Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond","day":"01","author":[{"first_name":"Florian","full_name":"Pauler, Florian","last_name":"Pauler","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"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"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","first_name":"Simon"}],"type":"journal_article","publisher":"Elsevier","isi":1,"publication":"Neurochemistry International","department":[{"_id":"SiHi"}],"quality_controlled":"1","intvolume":"       145","status":"public","month":"05","date_created":"2021-02-23T12:31:43Z"}]