GSE161930
Distinct roles for ATP-dependent chromatin remodeling enzymes in nucleotide excision repair in yeast
Nucleosomes are a significant barrier to the repair of UV damage because they impede damage recognition by nucleotide excision repair (NER). The RSC and SWI/SNF chromatin remodelers function in cells to promote DNA access by moving or evicting nucleosomes and both have been linked to NER in yeast. Here, we report genome-wide repair maps of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast cells lacking RSC or SWI/SNF activity. Our data indicate that SWI/SNF is not generally required for NER, but instead promotes repair of CPD lesions at specific yeast genes. In contrast, mutation or depletion of RSC subunits causes a general defect in NER across the yeast genome. Our data indicate that RSC is required for repair not only in nucleosomal DNA, but also neighboring linker DNA and nucleosome-free regions (NFRs). Furthermore, our data indicate that RSC plays a direct role in transcription coupled-NER (TC-NER) of transcribed DNA. These findings help to define the specific genomic and chromatin contexts in which each chromatin remodeler functions in DNA repair, and indicate that RSC plays a unique function in facilitating repair by both NER subpathways. Overall design: UV-induced CPD lesions were mapped in yeast cells both Immediately after UV damage formation (0hr time point) and following two hours of repair (2hr time point) using the CPD-seq method. Repair of CPD lesions was measured in both wild-type (WT) yeast and yeast cells mutated or depleted for subunits of the SWI/SNF or RSC ATP-dependent chromatin remodeling complexes.