A non-canonical BRD9-containing BAF chromatin remodeling complex regulates naive pluripotency in mouse embryonic stem cells

Jovylyn Gatchalian, Shivani Malik, Josephine Ho, Dong-Sung Lee, Timothy W. R. Kelso, Maxim N. Shokhirev, Jesse R. Dixon and Diana C. Hargreaves ()
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Jovylyn Gatchalian: Salk Institute for Biological Studies
Shivani Malik: Salk Institute for Biological Studies
Josephine Ho: Salk Institute for Biological Studies
Dong-Sung Lee: Salk Institute for Biological Studies
Timothy W. R. Kelso: Salk Institute for Biological Studies
Maxim N. Shokhirev: Salk Institute for Biological Studies
Jesse R. Dixon: Salk Institute for Biological Studies
Diana C. Hargreaves: Salk Institute for Biological Studies

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: Abstract The role of individual subunits in the targeting and function of the mammalian BRG1-associated factors (BAF) complex in embryonic stem cell (ESC) pluripotency maintenance has not yet been elucidated. Here we find that the Bromodomain containing protein 9 (BRD9) and Glioma tumor suppressor candidate region gene 1 (GLTSCR1) or its paralog GLTSCR1-like (GLTSCR1L) define a smaller, non-canonical BAF complex (GBAF complex) in mouse ESCs that is distinct from the canonical ESC BAF complex (esBAF). GBAF and esBAF complexes are targeted to different genomic features, with GBAF co-localizing with key regulators of naive pluripotency, which is consistent with its specific function in maintaining naive pluripotency gene expression. BRD9 interacts with BRD4 in a bromodomain-dependent fashion, which leads to the recruitment of GBAF complexes to chromatin, explaining the functional similarity between these epigenetic regulators. Together, our results highlight the biological importance of BAF complex heterogeneity in maintaining the transcriptional network of pluripotency.

Date: 2018
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DOI: 10.1038/s41467-018-07528-9

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