ABSTRACT
Membrane permeability was evaluated in several SOS-deficient strains. Great heat sensitivity was observed in all the lexA (Ind-) strains, which was associated to an increase in membrane permeability (up to 120 per cent increase above the wild-type control), as assayed by the crystal violet (CV) growth inhibition. After irradiation with a single UV dose (75 J.m-2 delivered to wild-type and 2 J.m-2 to the lex A3 strain), survival was followed by plating cells in both nutrient and membrane permeability-selective (nutrient + CV) media and a great lethality due to CV was observed in a lexA mutant, which appeared to be about 100 times more sensitive to CV compared to its wild-type parent stain. The decreased membrane integrity found in the lex A-deficient strains suggests that LexA protein and/or LexA-repressed genes may interact with the bacterial membrane, which could be the location of SOS events