| Literature DB >> 2115878 |
Abstract
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.Entities:
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Year: 1990 PMID: 2115878 PMCID: PMC213313 DOI: 10.1128/jb.172.8.4719-4720.1990
Source DB: PubMed Journal: J Bacteriol ISSN: 0021-9193 Impact factor: 3.490