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.

SWI/SNF 亚家族重塑剂（SWI/SNF 和 RSC）通常通过置换或驱逐启动子区域的核小体来促进基因表达。它们的作用产生了一个核小体耗尽区域，在那里转录机制可以访问 DNA。它们的功能已被证明对于诱导应激反应转录程序至关重要。尽管 SWI/SNF 和 RSC 复合物在热休克反应基因转录调控中的作用得到了很好的研究，但它们在其他途径中的参与，如未折叠蛋白反应 (UPR) 和蛋白质质量控​​制 (PQC) 却鲜为人知。该研究表明，SWI/SNF 占据 UPR、HSP 和 PQC 基因的启动子以响应未折叠蛋白应激，其在 UPR 启动子处的募集取决于 Hac1 转录因子和其他表观遗传因子，如 Ada2 和 Ume6。SWI/SNF'的中断 s 活性不影响这些启动子的重塑或基因表达。然而，RSC 和 SWI/SNF 的失活共同减少了大多数测试的 UPR、HSP 和 PQC 基因的诱导。此外，RSC 和 SWI/SNF 共定位在这些启动子上，表明这两个重塑子在功能上合作以在蛋白毒性条件下诱导应激反应基因。