Membrane permeability and sensitivity to lethal heat are affected by lexA and recA mutations in Escherichia coli K12.
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% 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 lexA3 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 strain. The decreased membrane integrity found in the lexA-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.
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Laboratório de Radiobiologia Molecular, Instituto de Biofisica Carlos Chag Filho, Universidade Federal do Rio de Janeiro, Brasil.
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D001426:Bacterial Proteins / Q000235:genetics*; D002463:Cell Membrane Permeability; D004926:Escherichia coli / Q000235:genetics / Q000528:radiation effects*; D005840:Gentian Violet; D006358:Hot Temperature; D009154:Mutation; D011938:Rec A Recombinases / Q000235:genetics*; D012097:Repressor Proteins / Q000235:genetics*; D013014:SOS Response, Genetics; D012697:Serine Endopeptidases; D000099160:LexA Repressor Protein
D001426:Bacterial Proteins; D005840:Gentian Violet; D011938:Rec A Recombinases; D012097:Repressor Proteins; D012697:Serine Endopeptidases; D000099160:LexA Repressor Protein