Mutagenic DNA repair in Streptomyces.
Streptomyces fradiae JS6 (mcr-6) is defective in the repair of potentially lethal damage to DNA induced by mitomycin C (MC), hydroxylamine (NH2OH), methyl methanesulfonate (MMS), 4-nitroquinoline 1-oxide (NQO), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and ultraviolet light (UV), but it exhibits nearly normal sensitivity to ethyl methanesulfonate (EMS)-induced lethality. JS6 is substantially less mutable by MNNG, MMS, NQO, UV, NH2OH, and also EMS than is the parental strain. A spontaneous revertant of JS6 showed wild-type levels of resistance to all of these agents and wild-type levels of induced mutagenesis, indicating that a single mutation caused the multiple traits displayed by JS6. The mcr-6 gene product thus appears to control an error-prone (mutagenic) DNA repair system. Mediation of EMS mutagenesis by an error-prone repair pathway in S. fradiae, rather than by direct mispairing as in Escherichia coli, suggests that the streptomycetes have evolved more efficient error-avoidance mechanisms than those commonly observed in the single-celled eubacteria.
D004260:DNA Repair / Q000187:drug effects; D004269:DNA, Bacterial / Q000235:genetics / Q000378:metabolism; D005020:Ethyl Methanesulfonate / Q000494:pharmacology; D009153:Mutagens / Q000494:pharmacology; D009154:Mutation; D013302:Streptomyces / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism
D004269:DNA, Bacterial; D009153:Mutagens; D005020:Ethyl Methanesulfonate