Abstract
A strong chronic induction of the SOS response system occurs in E. coli BW535, a strain defective in nth, nfo and xth genes, and hence severely deficient in the repair of abasic sites in DNA. This was shown here by visualization of filamentous growth of the BW535 strain and by measuring the level of beta-galactosidase expressed in BW535/pSK1002 in comparison to the AB1157/pSK1002 strain. The plasmid pSK1002 bears an umuC::lacZ fusion in which lacZ is under the control of the umuC promoter and regulated under the SOS regulon. Increases in the expression of beta-galactosidase occur in BW535 without any exogenous SOS inducer. Chronic induction of the SOS response was observed previously in E. coli strains bearing mutations in certain genes that have mutator activity and BW535 is a moderate mutator strain. However, not all mutators show this property, since chronic induction of SOS was not observed in mutT or mutY mutators. MutT and MutY proteins, when active, protect bacteria from mutations induced by 8-oxoG lesions in DNA. This suggests that accumulation of abasic sites, but not 8-oxoG residues in DNA, induce the SOS response.
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