In preparation for the unique segregation of homologs at the first meiotic division, chromosomes undergo dramatic changes. The meiosis-specific sister chromatid cohesins Rec8 and Rec11 of Schizosaccharomyces pombe are recruited around the time of premeiotic replication, and Rec10, a component of meiosis-specific linear elements, is subsequently added. Here we report that Rec10 is essential for meiosis-specific DNA breakage by Rec12 (Spo11 homolog) and for meiotic recombination. DNA breakage and recombination also depend on the Rec8 and Rec11 cohesins, strictly in some genomic intervals but less so in others. Thus, in addition to their previously recognized role in meiotic chromosome segregation, cohesins have a direct role, as do linear element components, in meiotic recombination by enabling double-strand DNA break formation by Rec12. Our results reveal a pathway, whose regulation is significantly different from that in the distantly related yeast Saccharomyces cerevisiae, for meiosis-specific chromosome differentiation and high-frequency recombination.linear elements ͉ meiotic recombination ͉ regional specificity T he cardinal feature of meiosis is the reduction of chromosome number from diploid to haploid. Although chromosomes are replicated only once in meiosis, there are two nuclear divisions. In the first division (meiosis I, or MI) homologs, rather than sister chromatids, segregate from each other, a process that requires mutual recognition of homologs. Specific recognition is provided by high-frequency meiotic recombination, normally between allelic positions on homologs rather than sister chromatids. Recombination provides physical connections between homologs, in the form of one or more crossovers, which allow tension to form when homologs are properly positioned to segregate to opposite poles of the cell at MI. At the second division (meiosis II) sister centromeres segregate from each other, as in a normal mitotic division.The unique behavior of chromosomes during meiosis requires certain meiosis-specific proteins, collectively called chromosomal core proteins, that modify sister chromatid cohesion, homolog juxtaposition and segregation, recombination, and perhaps replication. In the fission yeast Schizosaccharomyces pombe, the meiosis-specific cohesins Rec8 and Rec11 are recruited to chromosomes at or about the time of premeiotic replication (1, 2). Rec8 and Rec11 share sequence similarity with the S. pombe mitotic cohesins Rad21 and Psc3, respectively; rec8 and rec11 mutants manifest defects in meiotic sister chromatid cohesion and homolog segregation (1-3). Many organisms express a meiosis-specific Rec8 protein; like S. pombe, mice and humans express in addition a meiosis-specific Rec11-like protein, called STAG3, although the distantly related budding yeast Saccharomyces cerevisiae does not (4). Despite their important roles in chromosome segregation, the rec8 and rec11 genes were first identified by mutations that strongly reduce meiotic recombination at ade6 (5). These observations indicate a cl...
Meiosis is a specialized form of cell division by which sexually reproducing diploid organisms generate haploid gametes. During a long prophase, telomeres cluster into the bouquet configuration to aid chromosome pairing, and DNA replication is followed by high levels of recombination between homologous chromosomes (homologs). This recombination is important for the reductional segregation of homologs at the first meiotic division; without further replication, a second meiotic division yields haploid nuclei. In the fission yeast Schizosaccharomyces pombe, we have deleted 175 meiotically upregulated genes and found seven genes not previously reported to be critical for meiotic events. Three mutants (rec24, rec25, and rec27) had strongly reduced meiosis-specific DNA double-strand breakage and recombination. One mutant (tht2) was deficient in karyogamy, and two (bqt1 and bqt2) were deficient in telomere clustering, explaining their defects in recombination and segregation. The moa1 mutant was delayed in premeiotic S phase progression and nuclear divisions. Further analysis of these mutants will help elucidate the complex machinery governing the special behavior of meiotic chromosomes.
During meiosis, the formation of viable haploid gametes from diploid precursors requires that each homologous chromosome pair be properly segregated to produce an exact haploid set of chromosomes. Genetic recombination, which provides a physical connection between homologous chromosomes, is essential in most species for proper homologue segregation. Nevertheless, recombination is repressed specifically in and around the centromeres of chromosomes, apparently because rare centromeric (or pericentromeric) recombination events, when they do occur, can disrupt proper segregation and lead to genetic disabilities, including birth defects. The basis by which centromeric meiotic recombination is repressed has been largely unknown. We report here that, in fission yeast, RNAi functions and Clr4-Rik1 (histone H3 lysine 9 methyltransferase) are required for repression of centromeric recombination. Surprisingly, one mutant derepressed for recombination in the heterochromatic mating-type region during meiosis and several mutants derepressed for centromeric gene expression during mitotic growth are not derepressed for centromeric recombination during meiosis. These results reveal a complex relation between types of repression by heterochromatin. Our results also reveal a previously undemonstrated role for RNAi and heterochromatin in the repression of meiotic centromeric recombination and, potentially, in the prevention of birth defects by maintenance of proper chromosome segregation during meiosis.chromosome segregation | meiosis | Schizosaccharomyces pombe | DSB formation | genetic separation of heterochromatin functions
Previously isolated Schizosaccharomyces pombe swi5 mutants are defective in mitotic mating-type switching and in repair of meiotic recombination-related DNA double-strand breaks. Here, we identify the swi5 gene, which encodes an 85-amino-acid polypeptide, similar to Sae3 of Saccharomyces cerevisiae, with an N-terminal predicted coiled-coil domain. A swi5 complete deletion mutant had normal mitotic growth rate but was hypersensitive to DNA-damaging agents and defective in mating-type switching. In meiosis, recombinant frequencies were reduced by a factor of .01ف The swi5 deletion strongly reduced the viable spore yields of mutants lacking Rhp55 or Rhp57, proteins thought to aid joint molecule formation. Furthermore, the swi5 deletion strongly suppressed the low viable spore yield of mutants lacking Mus81•Eme1, which resolves joint molecules such as Holliday junctions. These and previous results indicate that the small Swi5 polypeptide acts in a branched pathway of joint molecule formation to repair meiotic DNA breaks.
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