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Identification of new genes required for meiotic recombination in Saccharomyces cerevisiae

Department of Biology, Faculty of Science, Osaka University, Japan.
Genetics (Impact Factor: 4.87). 02/1993; 133(1):51-66.
Source: PubMed

ABSTRACT Mutants defective in meiotic recombination were isolated from a disomic haploid strain of Saccharomyces cerevisiae by examining recombination within the leu2 and his4 heteroalleles located on chromosome III. The mutants were classified into two new complementation groups (MRE2 and MRE11) and eight previously identified groups, which include SPO11, HOP1, REC114, MRE4/MEK1 and genes in the RAD52 epistasis group. All of the mutants, in which the mutations in the new complementation groups are homozygous and diploid, can undergo premeiotic DNA synthesis and produce spores. The spores are, however, not viable. The mre2 and mre11 mutants produce viable spores in a spo13 background, in which meiosis I is bypassed, suggesting that these mutants are blocked at an early step in meiotic recombination. The mre2 mutant does not exhibit any unusual phenotype during mitosis and it is, thus, considered to have a mutation in a meiosis-specific gene. By contrast, the mre11 mutant is sensitive to damage to DNA by methyl methanesulfonate and exhibits a hyperrecombination phenotype in mitosis. Among six alleles of HOP1 that were isolated, an unusual pattern of intragenic complementation was observed.

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    • "However, there are mutants of the MRN(X) complex that are competent for Spo11 cleavage, but which are unable to remove the covalently bound Spo11 protein. These include alleles of Rad50 (termed rad50-S, (Cao et al. 1990)) and nuclease-deficient alleles of Mre11 (Ajimura et al. 1993; Moreau et al. 1999). Interestingly, the same phenotype is seen in null alleles of Sae2 (Keeney and Kleckner 1995; Prinz et al. 1997). "
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    • "Our functional analyses of a comprehensive histone point mutant library showed 90 MMS-sensitive mutants (Matsubara et al. 2007; Sakamoto et al. 2009). As most HR mutants show MMS sensitivity (Ajimura et al. 1993), these MMS-sensitive histone point mutants are potentially defective in one or more types of HR. Among these, H2A-S128A (see Introduction ) and H3-K56A (in this study) mutant cells are defective in HR. "
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    • "To determine whether the difference between C × C and C × P recombination is specific to rad52-Y66A, we tested another hyper-recombination mutant from the RAD52 epistasis group. Compared to a wild-type strain, spontaneous C × C recombination in an mre11Δ mutant is induced eight-to ten-fold [16]. This recombination rate is not increased further by the presence of the rad52-Y66A mutation (Table 1). "
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