1. Single-strand annealing mediates the conservative repair of double-strand DNA breaks in homologous recombination-defective germ cells of Caenorhabditis elegans
- Author
-
Woori Bae, Hyeon Sook Koo, Myon-Hee Lee, Seokbong Hong, Mi So Park, and Ha Kyeong Jeong
- Subjects
DNA Repair ,DNA repair ,Mutant ,DNA, Single-Stranded ,Biology ,Biochemistry ,03 medical and health sciences ,0302 clinical medicine ,Animals ,Missense mutation ,DNA Breaks, Double-Stranded ,Caenorhabditis elegans ,Caenorhabditis elegans Proteins ,Homologous Recombination ,Molecular Biology ,030304 developmental biology ,0303 health sciences ,Gene knockdown ,fungi ,Cell Biology ,biology.organism_classification ,Phenotype ,eye diseases ,In vitro ,Cell biology ,Germ Cells ,030220 oncology & carcinogenesis ,Mutation ,Homologous recombination - Abstract
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.
- Published
- 2019