抄録
Defects in the human XPV/POLH gene result in the variant form of the disease xeroderma pigmentosum (XP-V). The gene encodes DNA polymerase η (Polη), which catalyzes translesion synthesis (TLS) past UV-induced cyclobutane pyrimidine dimers (CPDs) and other lesions. To further understand the roles of Polη in multicellular organisms, we analyzed phenotypes caused by suppression of Caenorhabditis elegans POLH (Ce-POLH) by RNA interference (RNAi). F1 and F2 progeny from worms treated by Ce-POLH-specific RNAi grew normally, but F1 eggs laid by worms treated by RNAi against Ce-POLD, which encodes Polδ did not hatch. These results suggest that Polδ but not Polη is essential for C. elegans embryogenesis. Polη-targeted embryos UV-irradiated after egg laying were only moderately sensitive. In contrast, Polη-targeted embryos UV-irradiated prior to egg laying exhibited severe sensitivity, indicating that Polη contributes significantly to damage tolerance in C. elegans in early embryogenesis but only modestly at later stages. As early embryogenesis is characterized by high levels of DNA replication, Polη may confer UV resistance in C. elegans, perhaps by catalyzing TLS in early embryogenesis.
