期刊
GENETICS
卷 211, 期 2, 页码 503-513出版社
GENETICS SOCIETY AMERICA
DOI: 10.1534/genetics.118.301817
关键词
DNA damage checkpoint; replication fork arrest; Rpd3L; histone deacetylase; replication
资金
- Francis Crick Institute, from Cancer Research UK [FC001066]
- UK Medical Research Council [FC001066]
- Wellcome Trust [FC001066]
- European Molecular Biology Organization Long-Term Fellowship [ALTF 263-2011]
- Wellcome Trust Senior Investigator Award [106252/Z/14/Z]
- European Research Council [669424-CHROMOREP]
- Wellcome Trust [106252/Z/14/Z] Funding Source: Wellcome Trust
DNA replication forks that are stalled by DNA damage activate an S-phase checkpoint that prevents irreversible fork arrest and cell death. The increased cell death caused by DNA damage in budding yeast cells lacking the Rad53 checkpoint protein kinase is partially suppressed by deletion of the EXO1 gene. Using a whole-genome sequencing approach, we identified two additional genes, RXT2 and RPH1, whose mutation can also partially suppress this DNA damage sensitivity. We provide evidence that RXT2 and RPH1 act in a common pathway, which is distinct from the EXO1 pathway. Analysis of additional mutants indicates that suppression works through the loss of the Rpd3L histone deacetylase complex. Our results suggest that the loss or absence of histone acetylation, perhaps at stalled forks, may contribute to cell death in the absence of a functional checkpoint.
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