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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.
Mismatch repair-dependent mutagenesis in nondividing cells
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