Requirement for Homologous Recombination Functions for Expression of the mutA Mistranslator tRNA-Induced Mutator Phenotype in Escherichia coli

Abstract

Expression of the Escherichia coli mutA mutator phenotype requires recA, recB, recC, ruvA, and ruvC gene, but not recD, recF, recO, or recR genes. Thus, the recBCD-dependent homologous recombination system is a component of the signal pathway that activates an error-prone DNA polymerase in mutA cells.

The miaA Mutator Phenotype of Escherichia coli K-12 Requires Recombination Functions

“…The absence of the miaA mutator phenotype in both recA and recB mutants is consistent with the interpretation that this phenomenon depends on recombination functions, similar to TSM (1,17,28,29). Likewise, the miaA mutator phenotype and TSM were not dependent on polB and umuDC functions (Fig.…”

“…We could not detect the miaA mutator phenotype in CC104 miaA containing mutations in recA, recB, or recD, which are defective in homologous recombination functions (1,17,29) or in CC105 (AT3TA tester) as reported previously (6) (Fig. 2).…”

“…Only GC3TA transversion was increased in miaA mutants, whereas the mutA mutator phenotype, which has been hypothesized to induce TSM (17), led primarily to an increase in AT3TA transversions in tester strain CC105 (7.8-fold) as well as AT3CG and GC3TA transversions in tester strains CC101 and CC104 (5.1-fold and 3.7-fold, respectively) (23). The recD mutation abolished the miaA mutator phenotype, whereas a recD mutation failed to affect induction of TSM in mutA mutants (29). Finally, the miaA mutator phenotype was reduced, but not abolished, by the lexA(Ind Ϫ ) mutation, whereas TSM was not reduced in cells unable to induce the SOS response (28).…”

“…However, it was shown that the miaA mutator phenotype was not due to polarity on the expression of the downstream hfq gene, which encodes a pleiotropic regulator, or hflA-region genes, which encode a protease (32). Recently, Humayun and coworkers described a new pathway of mutagenesis that results in increased transversion mutations in response to translation stress (1,17,28,29). This translation stress-induced mutagenesis (TSM) pathway is induced in mutA mutants, which contain an anticodon mutation in the glyV tRNA gene that causes insertion of glycine instead of aspartic acid in proteins, such as the proofreading subunit of DNA polymerase (30,31).…”

“…This translation stress-induced mutagenesis (TSM) pathway is induced in mutA mutants, which contain an anticodon mutation in the glyV tRNA gene that causes insertion of glycine instead of aspartic acid in proteins, such as the proofreading subunit of DNA polymerase (30,31). Unexpectedly, the TSM pathway was recently shown to depend on recombination functions (1,28,29). In reviewing inducible mutagenic pathways in E. coli, Humayun hypothesized that the miaA mutator phenotype may be a manifestation of the TSM pathway (17).…”