| Literature DB >> 26655900 |
Ramanathan Narayanan1, Mehdi Pirouz2, Cemil Kerimoglu3, Linh Pham1, Robin J Wagener1, Kamila A Kiszka1, Joachim Rosenbusch1, Rho H Seong4, Michael Kessel2, Andre Fischer5, Anastassia Stoykova6, Jochen F Staiger7, Tran Tuoc8.
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.Entities:
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Year: 2015 PMID： 26655900 DOI： 10.1016/j.celrep.2015.10.046
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423