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Journal Article

Chromatin regulation by BAF170 controls cerebral cortical size and thickness.

MPS-Authors
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Tuoc,  T.C.
Research Group of Molecular Developmental Neurobiology, MPI for biophysical chemistry, Max Planck Society;

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Boretius,  S.
Biomedical NMR Research GmbH, MPI for biophysical chemistry, Max Planck Society;

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Pitulescu,  M. E.
Research Group of Developmental Biology, MPI for biophysical chemistry, Max Planck Society;

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Frahm,  J.
Biomedical NMR Research GmbH, MPI for biophysical chemistry, Max Planck Society;

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Stoykova,  A.
Research Group of Molecular Developmental Neurobiology, MPI for biophysical chemistry, Max Planck Society;

Fulltext (public)

1795866.pdf
(Publisher version), 4MB

Supplementary Material (public)

1795866_Supplement_1.pdf
(Supplementary material), 4MB

1795866_Supplement_2.xlsx
(Supplementary material), 370KB

Citation

Tuoc, T., Boretius, S., Sansom, S. N., Pitulescu, M. E., Frahm, J., Livesey, F. J., et al. (2013). Chromatin regulation by BAF170 controls cerebral cortical size and thickness. Developmental Cell, 25(3), 256-269. doi:10.1016/j.devcel.2013.04.005.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0013-F327-3
Abstract
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.