Ij. Fijalkowska et al., GENETIC REQUIREMENTS AND MUTATIONAL SPECIFICITY OF THE ESCHERICHIA-COLI SOS MUTATOR ACTIVITY, Journal of bacteriology, 179(23), 1997, pp. 7435-7445
To better understand the mechanisms of SOS mutagenesis in the bacteriu
m Escherichia coli, we have undertaken a genetic analysis of the SOS m
utator activity. The SOS mutator activity results from constitutive ex
pression of the SOS system in strains carrying a constitutively activa
ted RecA protein (RecA730). We show that the SOS mutator activity is n
ot enhanced in strains containing deficiencies in the uvr ABC nucleoti
de excision-repair system or the xth and nfo base excision-repair syst
ems. Further, recA730-induced errors are shown to be corrected by the
MutHLS-dependent mismatch-repair system as efficiently as the correspo
nding errors in the rec(+) background. These results suggest that the
SOS mutator activity does not reflect mutagenesis at so-called cryptic
lesions but instead represents an amplification of normally occurring
DNA polymerase errors. Analysis of the base-pair-substitution mutatio
ns induced by recA730 in a mismatch repair-deficient background shows
that both transition and transversion errors are amplified, although t
he effect is much larger for transversions than for transitions. Analy
sis of the mutator effect in various dnaE strains, including dnaE anti
mutators, as well as in proofreading-deficient dnaQ (mutD) strains sug
gests that in recA730 strains, two types of replication errors occur i
n parallel: (i) normal replication errors that are subject to both exo
nucleolytic proofreading and dnaE antimutator effects and (ii) recA730
-specific errors that are not susceptible to either proofreading or dn
aE antimutator effects. The combined data are consistent with a model
suggesting that in recA730 cells error-prone replication complexes are
assembled at sites where DNA polymerization is temporarily stalled, m
ost likely when a normal polymerase insertion error has created a poor
ly extendable terminal mismatch. The modified complex forces extension
of the mismatch largely at the exclusion of proofreading and polymera
se dissociation pathways. SOS mutagenesis targeted at replication-bloc
king DNA lesions likely proceeds in the same manner.