Relationship of methyl purines produced by MNNG in adenovirus 5 DNA to viral inactivation in repair-deficient (Mer-) human tumor cell strains.
Adenovirus 5 treated with MNNG (N-methyl-N'-nitro-N-nitrosoguanidine) has greater plaque-forming ability in cell strains having the Mer+ phenotype than in strains having the Mer- phenotype. MNNG-treated Mer- strains repair the N3-methyladenine (N3MeA) but not the O6-methylguanine (O6MeG) produced in their DNA, while MNNG-treated Mer+ strains repair both of these adducts. The fate of N7-methylguanine (another DNA adduct produced by MNNG) is similar in Mer+ and Mer- strains. We show in this paper that 2.3 +/- 0.4 O6MeG and 1.4 N3MeA per adenovirus genome correlate with one lethal hit when the survival assay is done using Mer- strains as viral hosts. We suggest that O6MeG is the lesion lethal to the virus.
D000260:Adenoviruses, Human / Q000187:drug effects* / Q000235:genetics; D000818:Animals; D004247:DNA / Q000378:metabolism; D004260:DNA Repair; D004279:DNA, Viral / Q000235:genetics*; D006367:HeLa Cells / Q000187:drug effects; D006801:Humans; D007700:Kinetics; D008297:Male; D008745:Methylation; D008769:Methylnitronitrosoguanidine / Q000378:metabolism / Q000633:toxicity*; D010641:Phenotype; D011687:Purines / Q000378:metabolism; D012474:Salmon; D013094:Spermatozoa; D010948:Viral Plaque Assay
D004279:DNA, Viral; D011687:Purines; D008769:Methylnitronitrosoguanidine; D004247:DNA