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Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/8778

Title: A role for the MutL homologue MLH2 in controlling heteroduplex formation and in regulating between two different crossover pathways in budding yeast
Authors: Abdullah, Mohammed F.F.
Hoffmann, Eva R.
Cotton, V.E.
Borts, Rhona H.
Issue Date: 2004
Publisher: Karger
Citation: Cytogenetic and Genome Research, 2004, 107(3-4), pp.180-190.
Abstract: Background and aims: Mismatch repair proteins play important roles during meiotic recombination in the budding yeast Saccharomyces cerevisiae and most eukaryotic organisms studied to date. To study the functions of the mismatch repair protein Mlh2p in meiosis, we constructed mlh2Δ strains and measured rates of crossing over, gene conversion, post-meiotic segregation and spore viability. We also analysed mlh1Δ, mlh3Δ, msh4Δ, msh5Δ, exo1Δ and mus81Δ mutant strains singularly and in various combinations. Results: Loss of MLH2 resulted in a small but significant decrease in spore viability and a significant increase in gene conversion frequencies but had no apparent effect on crossing over. Deletion of MLH2 in mlh3Δ, msh4Δ or msh5Δ strains resulted in significant proportion of the “lost” crossovers found in single deletion strains being regained in some genetic intervals. We and others propose that there are at least two pathways to generate crossovers in yeast (Ross-Macdonald and Roeder, 1994; Zalevsky et al., 1999; Khazanehdari and Borts, 2000; Novak et al., 2001; de los Santos et al., 2003). Most recombination intermediates are processed by the “major”, Msh4-dependent pathway, which requires the activity of Mlh1p/Mlh3p/Msh4p/Msh5p as well as a number of other proteins. The minor pathway(s) utilizes Mms4p/Mus81p. We suggest that the absence of Mlh2p allows some crossovers from the MSH4 pathway to traverse the MUS81-dependent pathway.
ISSN: 1424-8581 (Print)
1424-859X (Online)
Links: http://dx.doi.org/10.1159/000080596
http://hdl.handle.net/2381/8778
Type: Article
Description: The full-text of this item is currently not available on the LRA. The original published version is available on the publisher's website at: http://content.karger.com/ProdukteDB/produkte.asp?Aktion=BackIssues&ProduktNr=224037 DOI:10.1159/000080596
Appears in Collections:Published Articles, Dept. of Genetics

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