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Increased cortical size is essential to the enhanced intellectual capacity of primates during mammalian evolution. The mechanisms that control cortical size are largely unknown. Here, we show that mammalian BAF170, a subunit of the chromatin remodeling complex mSWI/SNF, is an intrinsic factor that controls cortical size. We find that conditional deletion of BAF170 promotes indirect neurogenesis by increasing the pool of intermediate progenitors (IPs) and results in an enlarged cortex, whereas cortex-specific BAF170 overexpression results in the opposite phenotype. Mechanistically, BAF170 competes with BAF155 subunit in the BAF complex, affecting euchromatin structure and thereby modulating the binding efficiency of the Pax6/REST-corepressor complex to Pax6 target genes that regulate the generation of IPs and late cortical progenitors. Our findings reveal a molecular mechanism mediated by the mSWI/SNF chromatin-remodeling complex that controls cortical architecture.

Original publication

DOI

10.1016/j.devcel.2013.04.005

Type

Journal article

Journal

Developmental cell

Publication Date

02/05/2013

Volume

25

Pages

256 - 269

Addresses

Research Group of Molecular Developmental Neurobiology, Department of Molecular Cell Biology, Max-Planck-Institute for Biophysical Chemistry, 37077 Göttingen, Germany.

Keywords

Cerebral Cortex, Neurons, Hela Cells, Chromatin, Animals, Mice, Transgenic, Humans, Mice, Multiprotein Complexes, Homeodomain Proteins, Eye Proteins, Nuclear Proteins, Histones, Transcription Factors, Repressor Proteins, Organ Size, Protein Interaction Mapping, Chromatin Assembly and Disassembly, DNA Methylation, Epigenesis, Genetic, Protein Binding, Female, Male, Paired Box Transcription Factors, Promoter Regions, Genetic, Neurogenesis, PAX6 Transcription Factor