DNA methylation alters the pattern of spontaneous mutation in Escherichia coli cells (mutD) defective in DNA polymerase III proofreading.
We have shown previously that dam mutants of Escherichia coli have a weak mutator phenotype which generates mostly transition mutations in the P22 mnt gene. In contrast, in mutD5 cells, which have a strong mutator phenotype, transversion mutations were the most prevalent. A dam-16 mutD5 strain, defective in both DNA polymerase III associated-proofreading and Dam-directed mismatch repair exhibits a strong mutator phenotype but, surprisingly, its mutation spectrum is similar to that of the dam rather than the mutD parent. The most likely explanation is that Dam-directed mismatch repair in the mutD5 strain corrects most of the potential transition mutations (therefore yielding transversions) in the newly synthesised strand. When the dam-16 allele is present together with mutD5 a reduced efficiency of repair as well as loss of strand discrimination and misdirected repair results in the appearance of transition mutations at high frequency.
Palmer
B R
BR
Department of Pharmacology, University of Massachusetts Medical School, Worcester 01655.
Marinus
M G
MG
D001435:Bacteriophages / Q000235:genetics; D003001:Cloning, Molecular; D004258:DNA Polymerase III / Q000235:genetics*; D004269:DNA, Bacterial / Q000378:metabolism*; D004926:Escherichia coli / Q000235:genetics* / Q000254:growth & development; D005798:Genes, Bacterial; D005814:Genes, Viral; D008745:Methylation; D009154:Mutation; D010641:Phenotype; D010957:Plasmids; D001616:beta-Galactosidase / Q000235:genetics
D004269:DNA, Bacterial; D004258:DNA Polymerase III; D001616:beta-Galactosidase