To explore the function of VIG-1 in , we analyzed the phenotypes of two deletion mutants: () and (). Both mutants exhibited phenotypes associated with genome instability, such as a high incidence of males (Him) and increased embryonic lethality. These phenotypes became more evident in succeeding generations, implying that the germline of accumulates DNA damage over generations. To examine whether causes a defect in the DNA damage response, we treated worms with UV or camptothecin, a specific topoisomerase I inhibitor. We observed that the embryonic survival of the mutants was reduced compared with that of the wild-type worms. Our results thus suggest that VIG-1 is required for maintaining genome stability in response to endogenous and exogenous genotoxic stresses.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6138327 | PMC |
http://dx.doi.org/10.1080/19768354.2018.1476410 | DOI Listing |
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