Escherichia coli strains with multiple DNA repair defects are hyperinduced for the SOS response.
Escherichia coli strains defective for the repair of apurinic/apyrimidinic sites and for the UvrABC excision repair pathway could be constructed if they also carried a mutation in ung, which encodes uracil glycosylase, or sulA, which encodes an SOS-inducible inhibitor of septation. The resultant strains were sensitive to alkylation damage and hyperinduced for the SOS response, but had unpredictable spontaneous mutation rates.
Foster
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Division of Environmental Health, Boston University School of Public Health, Massachusetts 02118.
D004260:DNA Repair; D004706:Endodeoxyribonucleases / Q000378:metabolism; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics*; D029968:Escherichia coli Proteins; D008741:Methyl Methanesulfonate / Q000494:pharmacology; D009154:Mutation; D013014:SOS Response, Genetics; D013045:Species Specificity; D014161:Transduction, Genetic; D001616:beta-Galactosidase / Q000235:genetics / Q000378:metabolism
D029968:Escherichia coli Proteins; D008741:Methyl Methanesulfonate; D004706:Endodeoxyribonucleases; C036385:endodeoxyribonuclease uvrABC; D001616:beta-Galactosidase