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Meiotic recombination in RAD54 mutants of Saccharomyces cerevisiae

Jacqueline Schmuckli-Maurer1 and Wolf-Dietrich Heyer1

(1)   Institute of General Microbiology, University of Bern, 3012 Bern, Switzerland, CH
(2)   Division of Biological Sciences, Section of Microbiology and Section of Molecular and Cellular Biology, University of California, Davis, CA 95616, USA, US
Abstract.   The Rad54 protein is an important component of the recombinational DNA repair pathway in vegetative Saccharomyces cerevisiae cells. Unlike those in other members of the RAD52 group, the meiotic defect in rad54 is rather mild, reducing spore viability only to 26%–65%. A consistently greater requirement for Rad54p during meiosis was observed in hybrid strains, suggesting that Rad54p has a certain role in interhomolog interactions. Such a role is probably minor as no recombination defects were found in the surviving gametes in three genetic intervals on chromosome V. Also, the spore viability pattern in tetrads did not reflect an increase in nondisjunction at meiosis I indicative of a meiotic recombination defect. We suggest that the meiotic defect of rad54 cells lies in the failure to repair meiosis-specific double-strand breaks outside the context of the highly differentiated pathway leading to interhomolog joint molecules and meiotic crossovers that ensure accurate segregation at meiosis I.
Received: 15 November 1999; in revised form: 11 January 2000 / Accepted: 11 January 2000

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Referenced by
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  1. San Filippo, Joseph (2008) Mechanism of Eukaryotic Homologous Recombination. Annual Review of Biochemistry 77(1)
    [CrossRef]
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