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Nucleic Acids Research 2005 33(16):5243-5249; doi:10.1093/nar/gki835
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Published online 15 September 2005

© The Author 2005. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oxfordjournals.org

Article

Inverted repeat-stimulated sister-chromatid exchange events are RAD1-independent but reduced in a msh2 mutant

Dilip K. Nag1,3,*, Michael Fasullo2,3, Zheng Dong2 and Ashlie Tronnes1

1Molecular Genetics Program, Wadsworth Center, Center for Medical Sciences 150 New Scotland Avenue, Albany, NY 12208, USA 2Ordway Research Institute, Wadsworth Center, Center for Medical Sciences 150 New Scotland Avenue, Albany, NY 12208, USA 3Department of Biomedical Sciences, School of Public Health, State University of New York Albany, NY 12201, USA

*To whom correspondence should be addressed. Tel: 518 473 6327; Fax: 518 474 3181; Email: dilip.nag{at}wadsworth.org

Received July 13, 2005. Revised August 29, 2005. Accepted August 29, 2005.

Inverted repeats (IRs) and trinucleotide repeats (TNRs) that have the potential to form secondary structures in vivo are known to cause genome rearrangements. Expansions of TNRs in humans are associated with several neurological disorders. Both IRs and TNRs stimulate spontaneous unequal sister-chromatid exchange (SCE) in yeast. Secondary structure-associated SCE events occur via double-strand break repair. Here we show that the rate of spontaneous IR-stimulated unequal SCE events in yeast is significantly reduced in strains with mutations in the mismatch repair genes MSH2 or MSH3, but unaffected by a mutation in the nucleotide excision-repair gene RAD1. Non-IR-associated unequal SCE events are increased in both MMR- and rad1-mutant cells; however, SCE events for both IR- and non-IR-containing substrates occur at a higher level in the exo1 background. Our results suggest that spontaneous SCE occurs by a template switching mechanism. Like IRs, TNRs have been shown to generate double-strand breaks (DSBs) in yeast. TNR expansions in mice are MSH2-dependent. Since IR-mediated SCE events are reduced in msh2 cells, we propose that TNR expansion mutations arise when DSBs are repaired using the sister or the homolog as a template.

Present address: Zheng Dong, Department of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, CA 90095, USA


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