DNA methylation alters the pattern of spontaneous mutation in Escherichia coli cells (mutD) defective in DNA polymerase III proofreading

UMMS Affiliation

Department of Biochemistry and Molecular Pharmacology

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Document Type



Bacteriophages; Cloning, Molecular; DNA Polymerase III; DNA, Bacterial; Escherichia coli; Genes, Bacterial; Genes, Viral; Methylation; *Mutation; Phenotype; Plasmids; beta-Galactosidase


Biochemistry, Biophysics, and Structural Biology | Pharmacology, Toxicology and Environmental Health


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.


Mutat Res. 1991 Sep;264(1):15-23.

Journal/Book/Conference Title

Mutation research

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