Mismatch repair in mammalian cells

Abstract

A vital process in maintaining a low genetic error rate is the removal of mismatched bases in DNA. The importance of this process in E. coli is demonstrated by the 100-1000 fold increase in mutation frequency observed in cells deficient in this repair system. Mismatches can arise as a consequence of recombination, errors in replication and as a result of spontaneous chemical deamination, the latter process resulting in an estimated twelve T:G mismatches per genome per day in mammalian cells. Recent studies, discussed here, provide evidence for the existence of specific mismatch repair systems in mammalian and human cells.

Functional assessment for elimination of mismatches in nuclear and whole cell extracts obtained from mouse and human blastocysts

“…Others have suggested that nicks may improve the repair efficiency and the repair is initiated from the nick [Thomas et al 1991;Holmes et al 1990;Fang and Modrich 1993;Umar et al 1994;Miller et al 1997;Taghian et al 1998]. Conflicting studies in monkey COS-7 (CV-1 in Origin and carrying the SV40 genetic material) cells suggested that nicks did not have an effect in directing the strand repair [Heywood and Burke 1990a;1990b]. Additional studies supported this by showing equal mismatch repair efficiency with nicked and intact plasmid DNA in in vivo studies [Lei et al 2004].…”