Nucleotide excision repair defect influences lethality and mutagenicity induced by Me-lex, a sequence-selective N3-adenine methylating agent in the absence of base excision repair

The role of nucleotide excision repair (NER) in Me-lex-induced toxicity and mutagenicity is explored, as it is known that NER acts on the basic sites in vivo in yeast and in vito assays. The findings indicate that in yeast NER can play a protective role against 3-MeA-mediated toxicity and mutagenicity, however the role of NER is appreciable only in a BER-defective background.