SRG3/mBAF155 stabilizes the SWI/SNF-like BAF complex by blocking CHFR mediated ubiquitination and degradation of its major components.

Biochem Biophys Res Commun

Research Center for Functional Cellulomics, Department of Biological Sciences, Institute for Molecular Biology and Genetics, Seoul National University, Seoul 151-742, Republic of Korea.

Published: February 2012

The murine SWI/SNF-like BAF complex is an ATP-dependent chromatin remodeling complex that functions as a transcriptional regulator in cell proliferation, differentiation and development. The SWI/SNF-like BAF complex consists of several components including core subunits such as BRG1, BAF155/SRG3, BAF47/SNF5/INI1, and BAF170. We have previously shown that the interaction between SRG3/mBAF155 and other components of the complex stabilizes them by attenuating their proteasomal degradation. However, it has not been known how the major components of the SWI/SNF-like BAF complex such as BRG1, SNF5, and BAF60a are targeted for the ubiquitination and degradation, and how SRG3/mBAF155 protects them from the degradation process. Here we report that CHFR interacts with BRG1, SNF5, and BAF60a of the SWI/SNF-like BAF complex and ubiquitinates them to target for degradation through a proteasome-mediated pathway, and that SRG3/mBAF155 stabilizes these components by blocking their interaction with CHFR.

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http://dx.doi.org/10.1016/j.bbrc.2012.01.057DOI Listing

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