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.
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Selected References
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