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Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):558-63. Epub 2006 Jan 5.

Biochemical basis for dominant mutations in the Saccharomyces cerevisiae MSH6 gene.

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1
Department of Medicine, Cancer Center, Ludwig Institute for Cancer Research, University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093-0669, USA.

Abstract

Here, the ATP-binding, ATP hydrolysis, mispair-binding, sliding clamp formation, and Mlh1-Pms1 complex interaction properties of dominant mutant Msh2-Msh6 complexes have been characterized. The results demonstrate two mechanisms for dominance. In one, seen with the Msh6-S1036P and Msh6-G1067D mutant complexes, the mutant complex binds mispaired bases, is defective for ATP-induced sliding clamp formation and assembly of ternary complexes with Mlh1-Pms1, and occludes mispaired bases from other mismatch repair pathways. In the second, seen with the Msh6-G1142D complex, the mutant complex binds mispaired bases and is defective for ATP-induced sliding clamp formation but assembles ternary complexes with Mlh1-Pms1 that either occlude the mispaired base or prevent Mlh1-Pms1 from acting in alternate mismatch repair pathways.

PMID:
16407100
PMCID:
PMC1334674
DOI:
10.1073/pnas.0510078103
[Indexed for MEDLINE]
Free PMC Article
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