Tuoc, Tran

[["dc.bibliographiccitation.firstpage","968"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Stem Cell Reports"],["dc.bibliographiccitation.lastpage","984"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Ulmke, Pauline Antonie"],["dc.contributor.author","Sakib, M. Sadman"],["dc.contributor.author","Ditte, Peter"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Xie, Yuanbin"],["dc.contributor.author","Mao, Xiaoyi"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2021-06-01T10:49:56Z"],["dc.date.available","2021-06-01T10:49:56Z"],["dc.date.issued","2021"],["dc.description.abstract","Intermediate progenitor cells (IPCs) are neocortical neuronal precursors. Although IPCs play crucial roles in corticogenesis, their molecular features remain largely unknown. In this study, we aimed to characterize the molecular profile of IPCs. We isolated TBR2-positive (+) IPCs and TBR2-negative (−) cell populations in the developing mouse cortex. Comparative genome-wide gene expression analysis of TBR2+ IPCs versus TBR2− cells revealed differences in key factors involved in chromatid segregation, cell-cycle regulation, transcriptional regulation, and cell signaling. Notably, mutation of many IPC genes in human has led to intellectual disability and caused a wide range of cortical malformations, including microcephaly and agenesis of corpus callosum. Loss-of-function experiments in cortex-specific mutants of Esco2, one of the novel IPC genes, demonstrate its critical role in IPC maintenance, and substantiate the identification of a central genetic determinant of IPC biogenesis. Our data provide novel molecular characteristics of IPCs in the developing mouse cortex."],["dc.identifier.doi","10.1016/j.stemcr.2021.03.008"],["dc.identifier.pmid","33798452"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86466"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/246"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/118"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B06: Die Rolle von RNA in Synapsenphysiologie und Neurodegeneration"],["dc.relation.issn","2213-6711"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","Molecular Profiling Reveals Involvement of ESCO2 in Intermediate Progenitor Cell Maintenance in the Developing Mouse Cortex"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Cell and Developmental Biology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Abbas, Eman"],["dc.contributor.author","Hassan, Mohamed A."],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Kiszka, Kamila"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Nguyen, Huu Phuc"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2021-09-01T06:38:19Z"],["dc.date.available","2021-09-01T06:38:19Z"],["dc.date.issued","2021"],["dc.description.abstract","Oligodendrocytes are responsible for axon myelination in the brain and spinal cord. Generation of oligodendrocytes entails highly regulated multistage neurodevelopmental events, including proliferation, differentiation and maturation. The chromatin remodeling BAF (mSWI/SNF) complex is a notable regulator of neural development. In our previous studies, we determined the indispensability of the BAF complex scaffolding subunits BAF155 and BAF170 for neurogenesis, whereas their role in gliogenesis is unknown. Here, we show that the expression of BAF155 and BAF170 is essential for the genesis of oligodendrocytes during brain development. We report that the ablation of BAF155 and BAF170 in the dorsal telencephalic (dTel) neural progenitors or in oligodendrocyte-producing progenitors in the ventral telencephalon (vTel) in double-conditional knockout (dcKO) mouse mutants, perturbed the process of oligodendrogenesis. Molecular marker and cell cycle analyses revealed impairment of oligodendrocyte precursor specification and proliferation, as well as overt depletion of oligodendrocytes pool in dcKO mutants. Our findings unveil a central role of BAF155 and BAF170 in oligodendrogenesis, and thus substantiate the involvement of the BAF complex in the production of oligodendrocytes in the forebrain."],["dc.description.abstract","Oligodendrocytes are responsible for axon myelination in the brain and spinal cord. Generation of oligodendrocytes entails highly regulated multistage neurodevelopmental events, including proliferation, differentiation and maturation. The chromatin remodeling BAF (mSWI/SNF) complex is a notable regulator of neural development. In our previous studies, we determined the indispensability of the BAF complex scaffolding subunits BAF155 and BAF170 for neurogenesis, whereas their role in gliogenesis is unknown. Here, we show that the expression of BAF155 and BAF170 is essential for the genesis of oligodendrocytes during brain development. We report that the ablation of BAF155 and BAF170 in the dorsal telencephalic (dTel) neural progenitors or in oligodendrocyte-producing progenitors in the ventral telencephalon (vTel) in double-conditional knockout (dcKO) mouse mutants, perturbed the process of oligodendrogenesis. Molecular marker and cell cycle analyses revealed impairment of oligodendrocyte precursor specification and proliferation, as well as overt depletion of oligodendrocytes pool in dcKO mutants. Our findings unveil a central role of BAF155 and BAF170 in oligodendrogenesis, and thus substantiate the involvement of the BAF complex in the production of oligodendrocytes in the forebrain."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3389/fcell.2021.619538"],["dc.identifier.pmid","34336815"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88908"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/409"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/151"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-455"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B06: Die Rolle von RNA in Synapsenphysiologie und Neurodegeneration"],["dc.relation.eissn","2296-634X"],["dc.relation.orgunit","Institut für Neuroanatomie"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.rights","CC BY 4.0"],["dc.title","Conditional Loss of BAF (mSWI/SNF) Scaffolding Subunits Affects Specification and Proliferation of Oligodendrocyte Precursors in Developing Mouse Forebrain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","256"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Developmental Cell"],["dc.bibliographiccitation.lastpage","269"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Tuoc, Tran Cong"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Sansom, Stephen N."],["dc.contributor.author","Pitulescu, Mara-Elena"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Livesey, Frederick J."],["dc.contributor.author","Stoykova, Anastassia"],["dc.date.accessioned","2017-09-07T11:44:52Z"],["dc.date.available","2017-09-07T11:44:52Z"],["dc.date.issued","2013"],["dc.description.abstract","Increased cortical size is essential to the enhanced intellectual capacity of primates during mammalian evolution. The mechanisms that control cortical size are largely unknown. Here, we show that mammalian BAF170, a subunit of the chromatin remodeling complex mSWI/SNF, is an intrinsic factor that controls cortical size. We find that conditional deletion of BAF170 promotes indirect neurogenesis by increasing the pool of intermediate progenitors (IPs) and results in an enlarged cortex, whereas cortex-specific BAF170 overexpression results in the opposite phenotype. Mechanistically, BAF170 competes with BAF155 subunit in the BAF complex, affecting euchromatin structure and thereby modulating the binding efficiency of the Pax6/REST-corepressor complex to Pax6 target genes that regulate the generation of IPs and late cortical progenitors. Our findings reveal a molecular mechanism mediated by the mSWI/SNF chromatin-remodeling complex that controls cortical architecture."],["dc.identifier.doi","10.1016/j.devcel.2013.04.005"],["dc.identifier.gro","3150356"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7111"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","1534-5807"],["dc.title","Chromatin Regulation by BAF170 Controls Cerebral Cortical Size and Thickness"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1011109"],["dc.bibliographiccitation.journal","Frontiers in Cell and Developmental Biology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.affiliation","Nguyen, Huong; \r\n1\r\nInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, Goettingen, Germany"],["dc.contributor.affiliation","Sokpor, Godwin; \r\n1\r\nInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, Goettingen, Germany"],["dc.contributor.affiliation","Parichha, Arpan; \r\n5\r\nTata Institute of Fundamental Research, Mumbai, India"],["dc.contributor.affiliation","Pham, Linh; \r\n1\r\nInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, Goettingen, Germany"],["dc.contributor.affiliation","Saikhedkar, Nidhi; \r\n5\r\nTata Institute of Fundamental Research, Mumbai, India"],["dc.contributor.affiliation","Xie, Yuanbin; \r\n1\r\nInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, Goettingen, Germany"],["dc.contributor.affiliation","Ulmke, Pauline Antonie; \r\n1\r\nInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, Goettingen, Germany"],["dc.contributor.affiliation","Rosenbusch, Joachim; \r\n1\r\nInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, Goettingen, Germany"],["dc.contributor.affiliation","Pirouz, Mehdi; \r\n6\r\nMax Planck Institute for Multidisciplinary Sciences, Goettingen, Germany"],["dc.contributor.affiliation","Behr, Rüdiger; \r\n8\r\nGerman Primate Center-Leibniz Institute for Primate Research, Goettingen, Germany"],["dc.contributor.affiliation","Stoykova, Anastassia; \r\n6\r\nMax Planck Institute for Multidisciplinary Sciences, Goettingen, Germany"],["dc.contributor.affiliation","Brand-Saberi, Beate; \r\n4\r\nDepartment of Anatomy and Molecular Embryology, Ruhr University Bochum, Bochum, Germany"],["dc.contributor.affiliation","Nguyen, Huu Phuc; \r\n3\r\nDepartment of Human Genetics, Ruhr University Bochum, Bochum, Germany"],["dc.contributor.affiliation","Staiger, Jochen F.; \r\n1\r\nInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, Goettingen, Germany"],["dc.contributor.affiliation","Tole, Shubha; \r\n5\r\nTata Institute of Fundamental Research, Mumbai, India"],["dc.contributor.affiliation","Tuoc, Tran; \r\n1\r\nInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, Goettingen, Germany"],["dc.contributor.author","Nguyen, Huong"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Parichha, Arpan"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Saikhedkar, Nidhi"],["dc.contributor.author","Xie, Yuanbin"],["dc.contributor.author","Ulmke, Pauline Antonie"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Pirouz, Mehdi"],["dc.contributor.author","Behr, Rüdiger"],["dc.contributor.author","Tuoc, Tran"],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Brand-Saberi, Beate"],["dc.contributor.author","Nguyen, Huu Phuc"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tole, Shubha"],["dc.date.accessioned","2022-11-01T10:17:17Z"],["dc.date.available","2022-11-01T10:17:17Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:12:49Z"],["dc.description.abstract","Early forebrain patterning entails the correct regional designation of the neuroepithelium, and appropriate specification, generation, and distribution of neural cells during brain development. Specific signaling and transcription factors are known to tightly regulate patterning of the dorsal telencephalon to afford proper structural/functional cortical arealization and morphogenesis. Nevertheless, whether and how changes of the chromatin structure link to the transcriptional program(s) that control cortical patterning remains elusive. Here, we report that the BAF chromatin remodeling complex regulates the spatiotemporal patterning of the mouse dorsal telencephalon. To determine whether and how the BAF complex regulates cortical patterning, we conditionally deleted the BAF complex scaffolding subunits BAF155 and BAF170 in the mouse dorsal telencephalic neuroepithelium. Morphological and cellular changes in the BAF mutant forebrain were examined using immunohistochemistry and\r\n in situ\r\n hybridization. RNA sequencing, Co-immunoprecipitation, and mass spectrometry were used to investigate the molecular basis of BAF complex involvement in forebrain patterning. We found that conditional ablation of BAF complex in the dorsal telencephalon neuroepithelium caused expansion of the cortical hem and medial cortex beyond their developmental boundaries. Consequently, the hippocampal primordium is not specified, the mediolateral cortical patterning is compromised, and the cortical identity is disturbed in the absence of BAF complex. The BAF complex was found to interact with the cortical hem suppressor LHX2. The BAF complex suppresses cortical hem fate to permit proper forebrain patterning. We provide evidence that BAF complex modulates mediolateral cortical patterning possibly by interacting with the transcription factor LHX2 to drive the LHX2-dependent transcriptional program essential for dorsal telencephalon patterning. Our data suggest a putative mechanistic synergy between BAF chromatin remodeling complex and LHX2 in regulating forebrain patterning and ontogeny."],["dc.description.sponsorship"," Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship"," National Institute of Diabetes and Digestive and Kidney Diseases http://dx.doi.org/10.13039/100000062"],["dc.identifier.doi","10.3389/fcell.2022.1011109"],["dc.identifier.pmid","36263009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/116773"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-605"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","2296-634X"],["dc.relation.issn","2296-634X"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","BAF (mSWI/SNF) complex regulates mediolateral cortical patterning in the developing forebrain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","226"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in Neuroscience"],["dc.bibliographiccitation.lastpage","25"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Castro-Hernandez, Ricardo"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2019-07-09T11:45:16Z"],["dc.date.available","2019-07-09T11:45:16Z"],["dc.date.issued","2018"],["dc.description.abstract","The generation of individual neurons (neurogenesis) during cortical development occurs in discrete steps that are subtly regulated and orchestrated to ensure normal histogenesis and function of the cortex. Notably, various gene expression programs are known to critically drive many facets of neurogenesis with a high level of specificity during brain development. Typically, precise regulation of gene expression patterns ensures that key events like proliferation and differentiation of neural progenitors, specification of neuronal subtypes, as well as migration and maturation of neurons in the developing cortex occur properly. ATP-dependent chromatin remodeling complexes regulate gene expression through utilization of energy fromATP hydrolysis to reorganize chromatin structure. These chromatin remodeling complexes are characteristically multimeric, with some capable of adopting functionally distinct conformations via subunit reconstitution to perform specific roles in major aspects of cortical neurogenesis. In this review, we highlight the functions of such chromatin remodelers during cortical development. We also bring together various proposed mechanisms by which ATP-dependent chromatin remodelers function individually or in concert, to specifically modulate vital steps in cortical neurogenesis."],["dc.identifier.doi","10.3389/fnins.2018.00226"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15084"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59196"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1662-453X"],["dc.relation.issn","1662-453X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","ATP-Dependent Chromatin Remodeling During Cortical Neurogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4618"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","4635"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Tuoc, Tran"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Nguyen, Huong"],["dc.contributor.author","Tonchev, Anton B."],["dc.contributor.author","Sun, Guoqiang"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Shi, Yanhong"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Stoykova, Anastassia"],["dc.date.accessioned","2017-09-07T11:46:21Z"],["dc.date.available","2017-09-07T11:46:21Z"],["dc.date.issued","2016"],["dc.description.abstract","The BAF chromatin remodeling complex plays an essential role in brain development. However its function in postnatal neurogenesis in hippocampus is still unknown. Here, we show that in postnatal dentate gyrus (DG), the BAF170 subunit of the complex is expressed in radial glial-like (RGL) progenitors and in cell types involved in subsequent steps of adult neurogenesis including mature astrocytes. Conditional deletion of BAF170 during cortical late neurogenesis as well as during adult brain neurogenesis depletes the pool of RGL cells in DG, and promotes terminal astrocyte differentiation. These derangements are accompanied by distinct behavioral deficits, as reflected by an impaired accuracy of place responding in the Morris water maze test, during both hidden platform as well as reversal learning. Inducible deletion of BAF170 in DG during adult brain neurogenesis resulted in mild spatial learning deficits, having a more pronounced effect on spatial learning during the reversal test. These findings demonstrate involvement of BAF170-dependent chromatin remodeling in hippocampal neurogenesis and cognition and suggest a specific role of adult neurogenesis in DG in adaptive behavior."],["dc.identifier.doi","10.1007/s12035-016-9948-5"],["dc.identifier.gro","3150498"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14191"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7269"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","0893-7648"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Ablation of BAF170 in developing and postnatal dentate gyrus affects neural stem cell proliferation, differentiation, and learning"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","109"],["dc.bibliographiccitation.journal","iScience"],["dc.bibliographiccitation.lastpage","126"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Narayanan, Ramanathan"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Castro Hernandez, Ricardo"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Ulmke, Pauline Antonie"],["dc.contributor.author","Kiszka, Kamila A."],["dc.contributor.author","Tonchev, Anton B."],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Seong, Rho H."],["dc.contributor.author","Teichmann, Ulrike"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2020-12-10T14:24:42Z"],["dc.date.available","2020-12-10T14:24:42Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.isci.2018.05.014"],["dc.identifier.issn","2589-0042"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72326"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Chromatin Remodeling BAF155 Subunit Regulates the Genesis of Basal Progenitors in Developing Cortex"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1006274"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLoS Genetics"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Bachmann, Christina"],["dc.contributor.author","Nguyen, Huong"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Rabe, Tamara I."],["dc.contributor.author","Patwa, Megha"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Seong, Rho H."],["dc.contributor.author","Ashery-Padan, Ruth"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2018-11-07T10:09:05Z"],["dc.date.available","2018-11-07T10:09:05Z"],["dc.date.issued","2016"],["dc.description.abstract","Neurogenesis is a key developmental event through which neurons are generated from neural stem/progenitor cells. Chromatin remodeling BAF (mSWI/SNF) complexes have been reported to play essential roles in the neurogenesis of the central nervous system. However, whether BAF complexes are required for neuron generation in the olfactory system is unknown. Here, we identified onscBAF and ornBAF complexes, which are specifically present in olfactory neural stem cells (oNSCs) and olfactory receptor neurons (ORNs), respectively. We demonstrated that BAF155 subunit is highly expressed in both oNSCs and ORNs, whereas high expression of BAF170 subunit is observed only in ORNs. We report that conditional deletion of BAF155, a core subunit in both onscBAF and ornBAF complexes, causes impaired proliferation of oNSCs as well as defective maturation and axonogenesis of ORNs in the developing olfactory epithelium (OE), while the high expression of BAF170 is important for maturation of ORNs. Interestingly, in the absence of BAF complexes in BAF155/BAF170 double-conditional knockout mice (dcKO), OE is not specified. Mechanistically, BAF complex is required for normal activation of Pax6-dependent transcriptional activity in stem cells/progenitors of the OE. Our findings unveil a novel mechanism mediated by the mSWI/SNF complex in OE neurogenesis and development."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.identifier.doi","10.1371/journal.pgen.1006274"],["dc.identifier.isi","000386069000012"],["dc.identifier.pmid","27611684"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13696"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39592"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1553-7404"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","mSWI/SNF (BAF) Complexes Are Indispensable for the Neurogenesis and Development of Embryonic Olfactory Epithelium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","303"],["dc.bibliographiccitation.journal","Neuroscience"],["dc.bibliographiccitation.lastpage","316"],["dc.bibliographiccitation.volume","463"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Kunwar, Ajaya J."],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Tuoc, Tran"],["dc.contributor.author","Rizzoli, Silvio O."],["dc.contributor.author","Tarabykin, Victor"],["dc.contributor.author","von Mollard, Gabriele Fischer"],["dc.contributor.author","Krieglstein, Kerstin"],["dc.contributor.author","Staiger, Jochen F."],["dc.date.accessioned","2021-06-01T09:41:26Z"],["dc.date.available","2021-06-01T09:41:26Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.neuroscience.2021.03.021"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84922"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","0306-4522"],["dc.title","Ablation of Vti1a/1b Triggers Neural Progenitor Pool Depletion and Cortical Layer 5 Malformation in Late-embryonic Mouse Cortex"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","655"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Annals of Clinical and Translational Neurology"],["dc.bibliographiccitation.lastpage","668"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Pringsheim, Milka"],["dc.contributor.author","Mitter, Diana"],["dc.contributor.author","Schröder, Simone"],["dc.contributor.author","Warthemann, Rita"],["dc.contributor.author","Plümacher, Kim"],["dc.contributor.author","Kluger, Gerhard"],["dc.contributor.author","Baethmann, Martina"],["dc.contributor.author","Bast, Thomas"],["dc.contributor.author","Braun, Sarah"],["dc.contributor.author","Büttel, Hans‐Martin"],["dc.contributor.author","Conover, Elizabeth"],["dc.contributor.author","Courage, Carolina"],["dc.contributor.author","Datta, Alexandre N."],["dc.contributor.author","Eger, Angelika"],["dc.contributor.author","Grebe, Theresa A."],["dc.contributor.author","Hasse‐Wittmer, Annette"],["dc.contributor.author","Heruth, Marion"],["dc.contributor.author","Höft, Karen"],["dc.contributor.author","Kaindl, Angela M."],["dc.contributor.author","Karch, Stephanie"],["dc.contributor.author","Kautzky, Torsten"],["dc.contributor.author","Korenke, Georg C."],["dc.contributor.author","Kruse, Bernd"],["dc.contributor.author","Lutz, Richard E."],["dc.contributor.author","Omran, Heymut"],["dc.contributor.author","Patzer, Steffi"],["dc.contributor.author","Philippi, Heike"],["dc.contributor.author","Ramsey, Keri"],["dc.contributor.author","Rating, Tina"],["dc.contributor.author","Rieß, Angelika"],["dc.contributor.author","Schimmel, Mareike"],["dc.contributor.author","Westman, Rachel"],["dc.contributor.author","Zech, Frank‐Martin"],["dc.contributor.author","Zirn, Birgit"],["dc.contributor.author","Ulmke, Pauline A."],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Tuoc, Tran"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Staudt, Martin"],["dc.contributor.author","Brockmann, Knut"],["dc.date.accessioned","2019-11-25T10:20:06Z"],["dc.date.accessioned","2021-10-27T13:21:31Z"],["dc.date.available","2019-11-25T10:20:06Z"],["dc.date.available","2021-10-27T13:21:31Z"],["dc.date.issued","2019"],["dc.description.abstract","Objective: FOXG1 syndrome is a rare neurodevelopmental disorder associated with heterozygous FOXG1 variants or chromosomal microaberrations in 14q12. The study aimed at assessing the scope of structural cerebral anomalies revealed by neuroimaging to delineate the genotype and neuroimaging phenotype associations. Methods: We compiled 34 patients with a heterozygous (likely) pathogenic FOXG1 variant. Qualitative assessment of cerebral anomalies was performed by standardized re-analysis of all 34 MRI data sets. Statistical analysis of genetic, clinical and neuroimaging data were performed. We quantified clinical and neuroimaging phenotypes using severity scores. Telencephalic phenotypes of adult Foxg1+/- mice were examined using immunohistological stainings followed by quantitative evaluation of structural anomalies. Results: Characteristic neuroimaging features included corpus callosum anomalies (82%), thickening of the fornix (74%), simplified gyral pattern (56%), enlargement of inner CSF spaces (44%), hypoplasia of basal ganglia (38%), and hypoplasia of frontal lobes (29%). We observed a marked, filiform thinning of the rostrum as recurrent highly typical pattern of corpus callosum anomaly in combination with distinct thickening of the fornix as a characteristic feature. Thickening of the fornices was not reported previously in FOXG1 syndrome. Simplified gyral pattern occurred significantly more frequently in patients with early truncating variants. Higher clinical severity scores were significantly associated with higher neuroimaging severity scores. Modeling of Foxg1 heterozygosity in mouse brain recapitulated the associated abnormal cerebral morphology phenotypes, including the striking enlargement of the fornix. Interpretation: Combination of specific corpus callosum anomalies with simplified gyral pattern and hyperplasia of the fornices is highly characteristic for FOXG1 syndrome."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2019"],["dc.identifier.doi","10.1002/acn3.735"],["dc.identifier.eissn","2328-9503"],["dc.identifier.issn","2328-9503"],["dc.identifier.pmid","31019990"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16705"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92029"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","2328-9503"],["dc.relation.issn","2328-9503"],["dc.relation.issn","2328-9503"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Structural brain anomalies in patients with FOXG 1 syndrome and in Foxg1+/− mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]