Sokpor, Godwin

[["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.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.journal","Frontiers in Molecular Neuroscience"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Nguyen, Huong"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Wagener, Robin"],["dc.contributor.author","Nguyen, Huu Phuc"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2021-08-12T07:45:46Z"],["dc.date.available","2021-08-12T07:45:46Z"],["dc.date.issued","2021"],["dc.description.abstract","Radial neuronal migration is a key neurodevelopmental event indispensable for proper cortical laminar organization. Cortical neurons mainly use glial fiber guides, cell adhesion dynamics, and cytoskeletal remodeling, among other discrete processes, to radially trek from their birthplace to final layer positions. Dysregulated radial migration can engender cortical mis-lamination, leading to neurodevelopmental disorders. Epigenetic factors, including chromatin remodelers have emerged as formidable regulators of corticogenesis. Notably, the chromatin remodeler BAF complex has been shown to regulate several aspects of cortical histogenesis. Nonetheless, our understanding of how BAF complex regulates neuronal migration is limited. Here, we report that BAF complex is required for neuron migration during cortical development. Ablation of BAF complex in the developing mouse cortex caused alteration in the cortical gene expression program, leading to loss of radial migration-related factors critical for proper cortical layer formation. Of note, BAF complex inactivation in cortex caused defective neuronal polarization resulting in diminished multipolar-to-bipolar transition and eventual disruption of radial migration of cortical neurons. The abnormal radial migration and cortical mis-lamination can be partly rescued by downregulating WNT signaling hyperactivity in the BAF complex mutant cortex. By implication, the BAF complex modulates WNT signaling to establish the gene expression program required for glial fiber-dependent neuronal migration, and cortical lamination. Overall, BAF complex has been identified to be crucial for cortical morphogenesis through instructing multiple aspects of radial neuronal migration in a WNT signaling-dependent manner."],["dc.description.abstract","Radial neuronal migration is a key neurodevelopmental event indispensable for proper cortical laminar organization. Cortical neurons mainly use glial fiber guides, cell adhesion dynamics, and cytoskeletal remodeling, among other discrete processes, to radially trek from their birthplace to final layer positions. Dysregulated radial migration can engender cortical mis-lamination, leading to neurodevelopmental disorders. Epigenetic factors, including chromatin remodelers have emerged as formidable regulators of corticogenesis. Notably, the chromatin remodeler BAF complex has been shown to regulate several aspects of cortical histogenesis. Nonetheless, our understanding of how BAF complex regulates neuronal migration is limited. Here, we report that BAF complex is required for neuron migration during cortical development. Ablation of BAF complex in the developing mouse cortex caused alteration in the cortical gene expression program, leading to loss of radial migration-related factors critical for proper cortical layer formation. Of note, BAF complex inactivation in cortex caused defective neuronal polarization resulting in diminished multipolar-to-bipolar transition and eventual disruption of radial migration of cortical neurons. The abnormal radial migration and cortical mis-lamination can be partly rescued by downregulating WNT signaling hyperactivity in the BAF complex mutant cortex. By implication, the BAF complex modulates WNT signaling to establish the gene expression program required for glial fiber-dependent neuronal migration, and cortical lamination. Overall, BAF complex has been identified to be crucial for cortical morphogenesis through instructing multiple aspects of radial neuronal migration in a WNT signaling-dependent manner."],["dc.identifier.doi","10.3389/fnmol.2021.687581"],["dc.identifier.pmid","34220450"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88547"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/408"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.publisher","Frontiers Media S.A."],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1662-5099"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Loss of BAF Complex in Developing Cortex Perturbs Radial Neuronal Migration in a WNT Signaling-Dependent Manner"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","100318"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","STAR Protocols"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Sakib, M. Sadman"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Nguyen, Huu Phuc"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2021-06-01T10:49:58Z"],["dc.date.available","2021-06-01T10:49:58Z"],["dc.date.issued","2021"],["dc.description.abstract","Cell sorting can be used to purify cell populations for cell type-specific molecular probing. Fluorescence-activated cell sorting (FACS) coupled with high-throughput sequencing affords molecular signature identification for specific cell types. FACS has many challenges that limit comprehensive cell purification from the brain, leading to incomplete molecular characterization. Here, we present the intranuclear immunostaining-based FACS protocol with several modified steps, which allows optimized nuclei/cell sorting from mouse or human embryonic cortical tissue for distinct downstream molecular investigation of basal intermediate progenitors."],["dc.identifier.doi","10.1016/j.xpro.2021.100318"],["dc.identifier.pmid","33554149"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86475"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/213"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/95"],["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","2666-1667"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","Intranuclear immunostaining-based FACS protocol from embryonic cortical tissue"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]