Previous studies in our laboratory used a papillation assay to identif
y a set of mutations in the E. coli dnaE gene that confer increased ac
curacy of DNA replication (antimutators). These antimutators were isol
ated as suppressors of the high mutability of a mismatch-repair-defect
ive mutL strain, in which the majority of mutations represent uncorrec
ted replication errors (mainly A . T --> G . C and G . C --> A . T tra
nsitions). In the present study, we have sought suppressors of the hig
h mutability of a mutT mutator strain. mutT strains produce a high fre
quency of A . T --> C . G transversions due to their lack of the mutT-
encoded 8-oxo-dGTPase, leading to a high frequency of A (8-oxoG) mispa
iring errors. Following localized mutagenesis of the dnaE-dnaQ region
of the chromosome, two strong suppressors of mutT mutability were obta
ined, both residing in the dnaE gene (dnaE940 and dnaE941). When subse
quently tested in a mutL strain, these two alleles also proved antimut
ators in this background, dnaE941 being significantly stronger than th
e previously isolated antimutators. The results suggest that the DNA p
olymerase may use similar mechanisms to discriminate against A .(8-oxo
G) transversion mispairs and A . C or T . G transition mispairs. The f
indings may also have significance for the interpretation of the antim
utator effect conferred by these dnaE alleles in a wild-type (mut(+))
background.