Journal Article

DZNE-2020-04577

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Loss of BAF (mSWI/SNF) Complexes Causes Global Transcriptional and Chromatin State Changes in Forebrain Development.

Narayanan, R. ; Pirouz, M. ; Kerimoglu, C.DZNE* ; Pham, L. ; Wagener, R. J. ; Kiszka, K. A. ; Rosenbusch, J. ; Seong, R. H. ; Kessel, M. ; Fischer, A.DZNE* ; Stoykova, A. ; Staiger, J. F. ; Tuoc, T. (Corresponding author)

2015
Elsevier [New York, NY]

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Please use a persistent id in citations: doi:10.1016/j.celrep.2015.10.046

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.

Keyword(s): DNA-Binding Proteins (MeSH) ; Animals (MeSH) ; Cell Differentiation (MeSH) ; Cell Proliferation (MeSH) ; Cells, Cultured (MeSH) ; Cerebellar Cortex: metabolism (MeSH) ; Chromatin: metabolism (MeSH) ; Chromosomal Proteins, Non-Histone: deficiency (MeSH) ; Chromosomal Proteins, Non-Histone: genetics (MeSH) ; Chromosomal Proteins, Non-Histone: metabolism (MeSH) ; DNA Helicases: metabolism (MeSH) ; Down-Regulation (MeSH) ; Embryo, Mammalian: metabolism (MeSH) ; Histone Demethylases: genetics (MeSH) ; Histone Demethylases: metabolism (MeSH) ; Histones: genetics (MeSH) ; Histones: metabolism (MeSH) ; Jumonji Domain-Containing Histone Demethylases: metabolism (MeSH) ; Mice (MeSH) ; Mice, Inbred C57BL (MeSH) ; Mice, Knockout (MeSH) ; Mice, Transgenic (MeSH) ; Neural Stem Cells: cytology (MeSH) ; Neural Stem Cells: metabolism (MeSH) ; Nuclear Proteins: metabolism (MeSH) ; Transcription Factors: deficiency (MeSH) ; Transcription Factors: genetics (MeSH) ; Transcription Factors: metabolism (MeSH) ; Chromatin ; Chromosomal Proteins, Non-Histone ; Histones ; Nuclear Proteins ; Smarcc1 protein, mouse ; Smarcc2 protein, mouse ; Transcription Factors ; Histone Demethylases ; Jumonji Domain-Containing Histone Demethylases ; Utx protein, mouse ; Kdm6b protein, mouse ; Smarca4 protein, mouse ; DNA Helicases

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Contributing Institute(s):

1. Epigenetics and Systems Medicine in Neurodegenerative Diseases (AG Fischer)

Research Program(s):

1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2015

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Database coverage:
; ; ; ; BIOSIS Previews ; Clarivate Analytics Master Journal List ; DOAJ Seal ; IF >= 5 ; JCR ; NCBI Molecular Biology Database ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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