Abstract
With acridine orange (AO) and monochromatic 460-nm light, the mutation rate of the wild-type strain of Escherichia coli (SP2) 3-fold higher than that of the endonuclease-deficinet strain WP2s ( uvrA). In addition, the mutation rates of the recombiination-deficient strains WP10 ( recA) and B s−1 ( uvrB lex A) were also about 3-fold less than that of teh wild-type straian. This observation is in striking contrast to the earlier results with AO and 500-nm light in which strains WP10 and B s−1 yielded mutation rates that were 12-fold and5-fold greater, respectively, that the wild-type response. The relatively large decrease in mutation reate when the uvrA endonuclease was absent together with structural condiseration in the binding of AO to DNA lead us to propose that the major lesions leading to mutations produced by 460-nm light in the presence of AO may be true DNA single-strand breaks that occur before DNA replication.
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More From: Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
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