E. coli MutS and MutL proteins participate in the methyl-directed mismatch repair system (MMRS), the very-short-.patch repair, the transcription-coupled nucleotide excision repair, and in the prevention of the homeologous recombination. In the MMRS, upon binding of MutH to the MutSL-DNA complex, the endonuclease activity of MutH is activated, and cleaves DNA 5` to the Dam hemimethylated -GATC- sequence in the unmethylated strand, directing repair to this strand. It has been shown using different experimental systems that overexpression of MutS or MutL is able to reduce the mutation rate in different bacteria. However, the mechanism(s) responsible for this effect is not known. It has been reported that this effect is not the result of an effect on the GO (8-Oxoguanine) repair system or on the RecD and RecG pathway. Here we show that an effect in the reduction of the mutation rate, after overexpression of MutS or MutL, is also produced in a dam mutant strain of E. coli. As the MMRS is non functional in this strain, our results indicate that the MMRS is probably not involved in the reduction of the mutation generated by overexpression of MutS or MutL. Experiments in order to determine the mechanism(s) responsible for this effect are under development.
