Mechanisms of ultraviolet-induced mutation. Mutational spectra in the Escherichia coli lacI gene for a wild-type and an excision-repair-deficient strain.

摘要: We have analyzed the DNA sequence changes in a total of 409 ultraviolet light-induced mutations lacI gene Escherichia coli: 227 Uvr+ and 182 UvrB- strain. Both differences similarities were observed. In both strains predominantly (60 to 75%) base substitutions, followed by smaller contributions single-base frameshifts, deletions frameshift hotspot mutations. The substitutions proved largely similar two but observed among Among transitions (72.5%) transversions (27.5%) largest single group was G.C----A.T (60% all substitutions). sites where occurred strongly correlated (97.5%) with sequences adjacent pyrimidines, indicating mutation targeted photoproducts. Comparable amounts at cytosine/cytosine (mixed) cytosine/thymine sites. From an analysis prevalence either 5' or 3' side dipyrimidine, we conclude that cyclobutane dimers (6-4) lesions may contribute mutation. Despite general similarity base-substitution spectra between wild-type excision-defective strains, number uniquely mutable Analysis their surrounding suggested that, addition damage directly site mutation, potential for nearby opposite-strand be important determining mutability site. losses. Inspection which frameshifts they resulted from mutagenesis, probably pyrimidine dimers. homodimers (TT CC) suggests formation involves local misalignment (slippage) base-pairing properties are partially retained While strain distributed over many different sites, more than half concentrated Ultraviolet as well (+/- TGGC positions 620 632) considered examples untargeted semitargeted mutagenesis. Hotspot showed increased contribution (-)TGGC relative (+)TGGC, light specifically promote loss four bases.(ABSTRACT TRUNCATED AT 400 WORDS)