The ATP-dependent SWI/SNF and RSC chromatin remodelers cooperatively induce unfolded protein response genes during endoplasmic reticulum stress

Abstract

The SWI/SNF subfamily remodelers (SWI/SNF and RSC) generally promote gene expression by displacing or evicting nucleosomes at the promoter regions. Their action creates a nucleosome-depleted region where transcription machinery accesses the DNA. Their function has been shown critical for inducing stress-responsive transcription programs. Although the role of SWI/SNF and RSC complexes in transcription regulation of heat shock responsive genes is well studied, their involvement in other pathways such as unfolded protein response (UPR) and protein quality control (PQC) is less known. This study shows that SWI/SNF occupies the promoters of UPR, HSP and PQC genes in response to unfolded protein stress, and its recruitment at UPR promoters depends on Hac1 transcription factor and other epigenetic factors like Ada2 and Ume6. Disruption of SWI/SNF's activity does not affect the remodeling of these promoters or gene expression. However, inactivation of RSC and SWI/SNF together diminishes induction of most of the UPR, HSP and PQC genes tested. Furthermore, RSC and SWI/SNF colocalize at these promoters, suggesting that these two remodelers functionally cooperate to induce stress-responsive genes under proteotoxic conditions.

Keywords: Chromatin remodeling complexes; ER stress; RSC; SWI/SNF; Transcription regulation; UPR.