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.