Requirement of the yeast MSH3 and MSH6 genes for MSH2-dependent genomic stability

Robert E. Johnson, Gopala K. Kovvali, Louise Prakash, Satya Prakash

Research output: Contribution to journalArticle

165 Scopus citations

Abstract

Defects in DNA mismatch repair result in instability of simple repetitive DNA sequences and elevated levels of spontaneous mutability. The human G/T mismatch binding protein, GTBP/p160, has been suggested to have a role in the repair of base-base and single nucleotide insertion-deletion mismatches. Here we examine the role of the yeast GTBP homolog, MSH6, in mismatch repair. We show that both MSH6 and MSH3 genes are essential for normal genomic stability. Interestingly, although mutations in either MSH3 or MSH6 do not cause the extreme microsatellite instability and spontaneous mutability observed in the msh2 mutant, yeast cells harboring null mutations in both the MSH3 and MSH6 genes exhibit microsatellite instability and mutability similar to that in the msh2 mutant. Results from epistasis analyses indicate that MSH2 functions in mismatch repair in conjunction with MSH3 or MSH6 and that MSH3 and MSH6 constitute alternate pathways of MSH2-dependent mismatch repair.

Original languageEnglish (US)
Pages (from-to)7285-7288
Number of pages4
JournalJournal of Biological Chemistry
Volume271
Issue number13
DOIs
StatePublished - Mar 29 1996

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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