Staiger, Jochen

[["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.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","1842"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","1854"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Narayanan, Ramanathan"],["dc.contributor.author","Pirouz, Mehdi"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Wagener, Robin J."],["dc.contributor.author","Kiszka, Kamila A."],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Seong, Rho H."],["dc.contributor.author","Kessel, Michael"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2017-09-07T11:54:50Z"],["dc.date.available","2017-09-07T11:54:50Z"],["dc.date.issued","2015"],["dc.description.abstract","BAF (Brg/Brm-associated factors) complexes play important roles in development and are linked to chromatin plasticity at selected genomic loci. Nevertheless, a full understanding of their role in development and chromatin remodeling has been hindered by the absence of mutants completely lacking BAF complexes. Here, we report that the loss of BAF155/BAF170 in double-conditional knockout (dcKO) mice eliminates all known BAF subunits, resulting in an overall reduction in active chromatin marks (H3K9Ac), a global increase in repressive marks (H3K27me2/3), and downregulation of gene expression. We demonstrate that BAF complexes interact with H3K27 demethylases (JMJD3 and UTX) and potentiate their activity. Importantly, BAF complexes are indispensable for forebrain development, including proliferation, differentiation, and cell survival of neural progenitor cells. Our findings reveal a molecular mechanism mediated by BAF complexes that controls the global transcriptional program and chromatin state in development."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1016/j.celrep.2015.10.046"],["dc.identifier.gro","3141775"],["dc.identifier.isi","000366047000012"],["dc.identifier.pmid","26655900"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12641"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/935"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.issn","2211-1247"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Loss of BAF (mSWI/SNF) Complexes Causes Global Transcriptional and Chromatin State Changes in Forebrain Development"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]