Previous Article | Next Article ![]()
Mol. Cell. Biol., 03 1996, 1085-1093, Vol 16, No. 3
A Datta, A Adjiri, L New, GF Crouse and S Jinks Robertson
Mismatch repair systems correct replication- and recombination- associated
mispaired bases and influence the stability of simple repeats. These
systems thus serve multiple roles in maintaining genetic stability in
eukaryotes, and human mismatch repair defects have been associated with
hereditary predisposition to cancer. In prokaryotes, mismatch repair
systems also have been shown to limit recombination between diverged
(homologous) sequences. We have developed a unique intron-based assay
system to examine the effects of yeast mismatch repair genes (PMS1, MSH2,
and MSH3) on crossovers between homologous sequences. We find that the
apparent antirecombination effects of mismatch repair proteins in mitosis
are related to the degree of substrate divergence. Defects in mismatch
repair can elevate homologous recombination between 91% homologous
substrates as much as 100-fold while having only modest effects on
recombination between 77% homologous substrates. These observations have
implications for genome stability and general mechanisms of recombination
in eukaryotes.
Copyright © 1996, American Society for Microbiology
Mitotic crossovers between diverged sequences are regulated by mismatch repair proteins in Saccaromyces cerevisiae
Graduate Program in Biochemistry and Molecular Biology, Emory University, Atlanta, Georgia 30322, USA.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»