Chromatin association between Srs2 and PCNA promotes inhibition of abscission in response to chromatin bridges. (A) Schematic representation of the Srs2 protein highlighting functional domains. The PIP and SIM regions are shown with their amino acid positions indicated. (B) Abscission dynamics of srs2 PIP and SIM mutants in the presence of catenated bridges. WT vs. top2-4, P < 0.0001; top2-4 vs. top2-4 srs2^SIM∆ and top2-4 srs2^PIP∆, P > 0.05; top2-4 vs. top2-4 srs2^PIP∆SIM∆, P < 0.0001, Mann–Whitney test. (C) Box plot showing the time from onset of contractile ring constriction to chromatin bridge segregation in the indicated strains. n = number of cells pooled from two independent experiments. Box indicates the median and interquartile range, whiskers are calculated with the Tukey method, and outliers are shown as dots. (D) Abscission dynamics of srs2-R337S (helicase-defective) in Top2-defective cells. WT vs. top2-4 srs2-R337S, <0.0001, Mann–Whitney test. (E) Inactivation of cold-sensitive PCNA (pol30-S115) in cells exposed to DNA replication stress. WT+HU vs. pol30-S11P+HU, P = 0.0004, Mann–Whitney test.