Rosenbusch, Joachim

[["dc.bibliographiccitation.firstpage","2575"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA"],["dc.bibliographiccitation.lastpage","2580"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","Kunwar, Ajaya J."],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Backofen, Bianca"],["dc.contributor.author","Browski, Sascha M."],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Schoening, Susanne"],["dc.contributor.author","Fleischmann, Thomas"],["dc.contributor.author","Krieglstein, Kerstin"],["dc.contributor.author","von Mollard, Gabriele Fischer"],["dc.date.accessioned","2018-11-07T08:59:16Z"],["dc.date.available","2018-11-07T08:59:16Z"],["dc.date.issued","2011"],["dc.description.abstract","Fusion between membranes is mediated by specific SNARE complexes. Here we report that fibroblasts survive the absence of the trans-Golgi network/early endosomal SNARE vti1a and the late endosomal SNARE vti1b with intact organelle morphology and minor trafficking defects. Because vti1a and vti1b are the only members of their SNARE subclass and the yeast homolog Vti1p is essential for cell survival, these data suggest that more distantly related SNAREs acquired the ability to function in endosomal traffic during evolution. However, absence of vti1a and vti1b resulted in perinatal lethality. Major axon tracts were missing, reduced in size, or misrouted in Vti1a(-/-) Vti1b(-/-) embryos. Progressive neurodegeneration was observed in most Vti1a(-/-) Vti1b(-/-) peripheral ganglia. Neurons were reduced by more than 95% in Vti1a(-/-) Vti1b(-/-) dorsal root and geniculate ganglia at embryonic day 18.5. These data suggest that special demands for endosomal membrane traffic could not be met in Vti1a(-/-) Vti1b(-/-) neurons. Vti1a(-/-) and Vti1b(-/-) single deficient mice were viable without these neuronal defects, indicating that they can substitute for each other in these processes."],["dc.identifier.doi","10.1073/pnas.1013891108"],["dc.identifier.isi","000287084500073"],["dc.identifier.pmid","21262811"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23851"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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.firstpage","97"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Developmental Neuroscience"],["dc.bibliographiccitation.lastpage","102"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Rahhal, Belal"],["dc.contributor.author","Heermann, Stephan"],["dc.contributor.author","Ferdinand, Anika"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Krieglstein, Kerstin"],["dc.date.accessioned","2018-11-07T08:33:04Z"],["dc.date.available","2018-11-07T08:33:04Z"],["dc.date.issued","2009"],["dc.description.abstract","Neurotrophic factors are well-recognized extracellular signaling molecules that regulate neuron development including neurite growth, survival and maturation of neuronal phenotypes in the central and peripheral nervous system. Previous studies have suggested that TGF-beta plays a key role in the regulation of neuron survival and death and potentiates the neurotrophic activity of several neurotrophic factors, most strikingly of GDNF. To test the physiological relevance of this finding, TGF-beta 2/GDNF double mutant (d-ko) mice were generated. Double mutant mice die at birth like single mutants due to kidney agenesis(GDNF / )and congential cyanosis (TGF-beta 2-/-), respectively. To test for the in vivo relevance of TCF-beta 2/GDNF cooperativity to regulate neuron survival, mesencephalic dopaminergic neurons, lumbar motoneurons, as well as neurons of the lumbar dorsal root ganglion and the superior cervical ganglion were investigated. No loss of mesencephalic dopaminergic neurons was observed in double mutant mice at E18.5. A partial reduction in neuron numbers was observed in lumbar motoneurons, sensory and sympathetic neurons in GDNF single mutants, which was further reduced in TGF-beta 2/GDNF double mutant mice at E18.5. However, TGF-beta 2 single mutant mice showed no loss of neurons. These data point towards a cooperative role of TGF-beta 2 and GDNF with regard to promotion of survival within the peripheral motor and sensory systems investigated. (C) 2008 ISDN. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ijdevneu.2008.08.003"],["dc.identifier.isi","000263387300013"],["dc.identifier.pmid","18824086"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17490"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","1873-474X"],["dc.relation.issn","0736-5748"],["dc.title","In vivo requirement of TGF-beta/GDNF cooperativity in mouse development: focus on the neurotrophic hypothesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","584"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecular and Cellular Neuroscience"],["dc.bibliographiccitation.lastpage","601"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Bohm, D."],["dc.contributor.author","Schwegler, H."],["dc.contributor.author","Kotthaus, L."],["dc.contributor.author","Nayernia, K."],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Kohler, M."],["dc.contributor.author","Rosenbusch, J."],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Flugge, G."],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T09:46:43Z"],["dc.date.available","2018-11-07T09:46:43Z"],["dc.date.issued","2002"],["dc.description.abstract","Aberrant reorganization of hippocampal mossy fibers occurs in human temporal lobe epilepsy and rodent epilepsy models. We generated a mouse model showing massive late-onset aberrant mossy fiber sprouting in the adult hippocampus. The mutation in this mouse model derives from an intronic insertion of transgene DNA in the mouse PLC-beta1 gene (PLC-beta1(TC)(-/-) mutation) leading to a splice mutation of the PLC-beta1 gene and a complete loss of downstream PLC-beta1 expression. PLC-beta1(TC)(-/-) mutants develop a loss of NMDA-receptors in the stratum oriens of region CA1, apoptotic neuronal death, and reduced hippocampal PKC activity. The phenotype of these mice further consists of a late-onset epileptiform hyperexcitability, behavioral modifications in a radial maze and in an open field, female nurturing defect, and male infertility. In the present study, we provide evidence that the arising of the behavioral phenotype in PLC-beta1(TC)(-/-) mice correlates in time with the development of the aberrant mossy fiber projections and that the disruption of the PLC-beta1-mediated signal transduction pathway may lead to a functional cholinergic denervation, which could cause hippocampal remodeling and, in consequence, epileptiform hyperexcitability."],["dc.identifier.doi","10.1006/mcne.2002.1199"],["dc.identifier.isi","000180026300006"],["dc.identifier.pmid","12504592"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34945"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","1044-7431"],["dc.title","Disruption of PLC-beta 1-mediated signal transduction in mutant mice causes age-dependent hippocampal mossy fiber sprouting and neurodegeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","8306"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","8327"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Abbas, Eman"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2020-12-10T14:14:27Z"],["dc.date.available","2020-12-10T14:14:27Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s12035-018-0987-y"],["dc.identifier.eissn","1559-1182"],["dc.identifier.issn","0893-7648"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71347"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Transcriptional and Epigenetic Control of Mammalian Olfactory Epithelium Development"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]