Abstract
The phenomenon of Cairnsian mutagenesis was studied inEscherichia coli mutants bearing mutations inmutS,mutL,recA andlexA genes. It is shown that development of resistance to exogenous valine could be used as an example of Cairnsian response. Strains defective inmutS andmutL show a high frequency of Cairnsian mutagenesis to valine resistance. The response inmutS mutants is dependent upon cleavability of the LexA protein whereas that inmutL is not. The latter is independent ofrecA also. The need for LexA protein cleavage inmutS mutants can be bypassed by over-production of the RecA protein due to arecA operator constitutive mutation. Genetic evidence is presented to show that the products ofmutS andmutL genes negativelycontrol two pathways of Cairnsian mutagenesis. Cairnsian response is also elicited whenmutS ormutL strains are grown under conditions wherein a required nutrient is present in sub-optimal concentrations. Random, unselected mutagenic events are likely to occur during or after Cairnsian mutagenesis provided the cells are SOS inducible.
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Dedicated to the memory of S.E. Luria
I have observed that adam13 (dam::Tn9) derivative of AB1157 is no better thandam + AB1157 in eliciting Cairnsian response. If Cairnsian response is the result of uncorrected mismatches, increasing the life span of mismatches (mutS/mutL) or correction of the wrong (parental) strand of mismatches (dam) will have the same consequence. That this is not so in Cairnsian response supports the notion outlined in this report that the role of the MutS and MutL products in Cairnsian mutagenesis is not simply to prolong the life span of mismatches.
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Jayaraman, R. Cairnsian mutagenesis inEscherichia coli: Genetic evidence for two pathways regulated bymutS andmutL genes. J. Genet. 71, 23–41 (1992). https://doi.org/10.1007/BF02927873
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DOI: https://doi.org/10.1007/BF02927873