RSC plays a direct role in transcription-coupled NER. (A) TC-NER efficiency is reduced in Sth1-AA cells relative to the WT-AA control, as reflected by the log ratio of unrepaired CPDs on the TS relative to the NTS being closer to zero (i.e., no repair asymmetry owing to TC-NER). CPD-seq data are for the 2-h repair time point relative to the 0-h control for approximately 5000 genes. (B) Same as panel A, except for rsc2Δ-mutant cells. (C) Schematic of RSC's potential roles in TC-NER. It is possible RSC may promote repair of the TS through GG-NER or may affect TC-NER indirectly (by altering RNA polymerase II [RNAP] transcription) or directly. (D,E) CPD-seq analysis examining the repair of CPDs on both DNA strands across approximately 5000 genes of the genome in GG-NER-deficient rad16Δ WT-AA and rad16Δ Sth1-AA cells treated with rapamycin. The fraction of CPDs remaining is calculated as the ratio of damage after 2 h of repair compared with the damage immediately following UV irradiation (0 h). (F) Same as panel A, except for GG-NER-deficient rad16Δ WT-AA and rad16Δ Sth1-AA cells. (G) Gene plot analysis of RNA polymerase II (Pol II) occupancy in Sth1-AA cells (left panel). Values calculated from log ratio of Rpb3 ChIP-seq data from Sth1-AA cells treated with rapamycin relative to the vehicle control (Kubik et al. 2018). Gene plot analysis of CPD repair on the TS of rad16Δ Sth1-AA cells. Left and right display relationship between RNA Pol II occupancy and unrepaired CPDs in each of the approximately 5000 genes mapped, ordered by decreasing Pol II occupancy in Sth1-AA-depleted cells.
