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. 2021 Jun;31(6):1047–1059. doi: 10.1101/gr.274373.120

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© 2021 Bohm et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see https://genome.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 1. — RSC is generally required for repair of CPD lesions in yeast, whereas SWI/SNF is not. (A,B) UV sensitivity of yeast mutants in the RSC (rsc1Δ and rsc2Δ) or SWI/SNF complex (snf6Δ). (C,D) UV sensitivity of rad26Δrsc2Δ and rad16Δrsc2Δ double mutants compared with single mutants. (E) Representative alkaline gel of CPD repair in WT and snf6Δ-mutant cells. Genomic DNA was isolated at the indicated time following damage induction with 100 J/m² UVC light and treated with or without (+/−) T4 endonuclease V. (F–I) Quantification of CPD repair in RSC or SWI/SNF mutants based on alkaline gel analysis. The percentage of CPDs repaired is plotted as the mean ± SEM of a minimum of three replicates. P-values were calculated using an unpaired t-test with Holm–Sidak correction for multiple hypothesis testing. (*) P ≤ 0.05.