期刊
DNA REPAIR
卷 75, 期 -, 页码 18-28出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.dnarep.2019.01.007
关键词
Double-strand DNA break; DNA repair; Homologous recombination; Single-strand annealing
资金
- National Research Foundation of Korea [2016R1D1A1B03934743]
- Brain Korea 21 (BK21) PLUS program
- National Research Foundation of Korea [2016R1D1A1B03934743] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
A missense mutation in C. elegans RAD-54, a homolog of RAD54 that operates in the homologous recombination (HR) pathway, was found to decrease ATPase activity in vitro. The hypomorphic mutation caused hypersensitivity of C. elegans germ cells to double-strand DNA breaks (DSBs). Although the formation of RAD-51 foci at DSBs was normal in both the mutant and knockdown worms, their subsequent dissipation was slow. The rad-54-deficient phenotypes were greatly aggravated when combined with an xpf-1 mutation, suggesting a conservative role of single-strand annealing (SSA) for DSB repair in HR-defective worms. The phenotypes of doubly-deficient rad-54;xpf-1 worms were partially suppressed by a mutation of lig-4, a nonhomologous end-joining (NHEJ) factor. In summary, RAD-54 is required for the dissociation of RAD-51 from DSB sites in C. elegans germ cells. Also, NHEJ and SSA exert negative and positive effects, respectively, on genome stability when HR is defective.
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