Non-growing quiescent cells face special challenges when repairing lesions produced by exogenous DNA damaging agents. These challenges include the global repression of transcription and translation and a compacted chromatin structure. We investigated how quiescent yeast cells regulated the repair of DNA lesions produced by UV irradiation. We found that UV lesions were excised and repaired in quiescent cells before their re-entry into S phase, and that lesion repair was correlated with high levels of Rad7, a recognition factor in the global genome repair sub-pathway of nucleotide excision repair (GGR-NER). UV exposure led to an increased frequency of mutations that included C->T transitions and T > A transversions. Mutagenesis was dependent on the error-prone translesion synthesis (TLS) DNA polymerase, Pol zeta, which was the only DNA polymerase present in detectable levels in quiescent cells. Across the genome of quiescent cells, UV-induced mutations showed an association with exons that contained H3K36 or H3K79 trimethylation but not with those bound by RNA polymerase II. Together, the data suggest that the distinct physiological state and chromatin structure of quiescent cells contribute to its regulation of UV damage repair.

中文翻译：

---

调节静态酵母细胞中的紫外线损伤修复。

当修复外源性DNA损伤剂产生的损伤时，非生长的静止细胞面临特殊挑战。这些挑战包括对转录和翻译的整体抑制以及紧凑的染色质结构。我们研究了静态酵母细胞如何调节紫外线照射产生的DNA损伤的修复。我们发现紫外线损伤在静止细胞中被切除并修复，然后再重新进入S期，并且损伤修复与高水平的Rad7相关，Rad7是核苷酸切除修复（GGR）的全球基因组修复子途径中的识别因子-NER）。紫外线暴露导致突变频率增加，包括C-> T转换和T> A转换。诱变取决于容易出错的跨病变合成（TLS）DNA聚合酶Pol Zeta，这是在静止细胞中可检测水平的唯一DNA聚合酶。在整个静止细胞的基因组中，紫外线诱导的突变显示与含有H3K36或H3K79三甲基化但不与RNA聚合酶II结合的外显子相关。总之，数据表明静态细胞的独特生理状态和染色质结构有助于其调节紫外线损伤修复。