In vivo repair of alkylating and oxidative DNA damage in the mitochondrial and nuclear genomes of wild-type and glycosylase-deficient Caenorhabditis elegans.

摘要: Base excision repair (BER) is an evolutionarily conserved DNA pathway that critical for of many the most common types damage generated both by endogenous metabolic pathways and exposure to exogenous stressors such as pollutants. Caenorhabditis elegans increasingly important model organism study damage-related processes including repair, genotoxicity, apoptosis, but BER not well understood in this organism, has previously been measured vivo. We report robust nuclear genome slightly slower removal from mitochondrial genome; cases rates are comparable those observed mammals. However we could detect no deficiency nth-1 strain, which carries a deletion only glycosylase yet described C. repairs oxidative damage. also failed increased lethality or growth inhibition nematodes after alkylating damage, suggesting existence at least one additional as-yet undetected glycosylase.