Mutagenic DNA repair in Escherichia coli. XII. Ultraviolet mutagenesis in excision-proficient umuC and lexA (ind-) bacteria as revealed by delayed photoreversal.
Streptomycin-resistant mutations are induced in excision-proficient umuC122::Tn5 bacteria given delayed photoreversal after u.v. light. The mutations occur after much earlier photoreversal than is found with the similar induction of tryptophan-independent mutations in excision-deficient umuC bacteria and the process is not markedly influenced by the presence of Casamino acids. The yield of mutants is between 25 and 40% of that found immediately after u.v. irradiation of isogenic umu+ bacteria. Mutagenesis is not inhibited by the presence of chloramphenicol after u.v. and before photoreversal when the bacteria have also been pretreated with chloramphenicol. Loss of photoreversibility of streptomycin-resistant mutations in umu+ excision-proficient bacteria also occurs during a similar period after u.v. and is similarly unaffected by Casamino acids and chloramphenicol. The results are interpreted on a 2-step model of error-prone repair in which a misincorporation step is followed by a lesion bypass step which requires induced levels of umuC gene product, the latter step being unnecessary when the pyrimidine dimer is removed by photoreversal after the misincorporation has taken place. Differences from the same phenomenon in excision-deficient bacteria are accounted for by the fact that in excision-proficient bacteria the mutation process is initiated by excision repair rather than during normal chromosomal replication. It is suggested that loss of photoreversibility in excision-proficient umu+ bacteria may reflect the misincorporation step only, thus explaining the apparent non-inducible nature of loss of photoreversibility previously reported. The bypass step alone requires induced levels of umuD,C gene products as is evidenced by the u.v.-induction of mutations in lexA102(ind-) bacteria after delayed photoreversal.(ABSTRACT TRUNCATED AT 250 WORDS)
Bridges
B A
BA
MRC Cell Mutation Unit, University of Sussex, Brighton, UK.
Sharif
F
F
D001426:Bacterial Proteins / Q000235:genetics*; D002701:Chloramphenicol / Q000494:pharmacology; D004260:DNA Repair / Q000528:radiation effects*; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects*; D007700:Kinetics; D008027:Light; D009154:Mutation; D012697:Serine Endopeptidases; D013307:Streptomycin / Q000494:pharmacology; D014466:Ultraviolet Rays; D000099160:LexA Repressor Protein
D001426:Bacterial Proteins; D002701:Chloramphenicol; D012697:Serine Endopeptidases; D013307:Streptomycin; D000099160:LexA Repressor Protein