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Mismatch repair-dependent mutagenesis in nondividing cells
Edited by Richard D. Kolodner, Ludwig Institute for Cancer Research, La Jolla, CA, and approved March 5, 2012 (received for review September 19, 2011)

Abstract
Mismatch repair (MMR) is a major DNA repair pathway in cells from all branches of life that removes replication errors in a strand-specific manner, such that mismatched nucleotides are preferentially removed from the newly replicated strand of DNA. Here we demonstrate a role for MMR in helping create new phenotypes in nondividing cells. We show that mispairs in yeast that escape MMR during replication can later be subject to MMR activity in a replication strand-independent manner in nondividing cells, resulting in either fully wild-type or mutant DNA sequence. In one case, this activity is responsible for what appears to be adaptive mutation. This replication strand-independent MMR activity could contribute to the formation of tumors arising in nondividing cells and could also contribute to mutagenesis observed during somatic hypermutation of Ig genes.
Footnotes
- ↵1To whom correspondence should be addressed. E-mail: gcrouse{at}biology.emory.edu.
Author contributions: Y.W.K. and G.F.C. designed research; G.P.R., N.V.R., G.B., and N.C.R. performed research; and G.F.C. wrote the paper.
The authors declare no conflict of interest.
This article is a PNAS Direct Submission.
This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1115361109/-/DCSupplemental.
Freely available online through the PNAS open access option.