Originally published as Genetics Published Articles Ahead of Print on October 8, 2006.

Genetics, Vol. 174, 1745-1754, December 2006, Copyright © 2006
doi:10.1534/genetics.106.058933

Centromere-Proximal Crossovers Are Associated With Precocious Separation of Sister Chromatids During Meiosis in Saccharomyces cerevisiae

Beth Rockmill^*, Karen Voelkel-Meiman^* and G. Shirleen Roeder^*,,1

^* Howard Hughes Medical Institute, Department of Molecular, Cellular and Developmental Biology and Department of Genetics, Yale University, New Haven, Connecticut 06520-8103

¹ Corresponding author: Howard Hughes Medical Institute, Department of Molecular, Cellular and Developmental Biology, Yale University, PO Box 208103, 266 Whitney Ave., New Haven, CT 06520-8103.
E-mail: shirleen.roeder{at}yale.edu

In most organisms, meiotic chromosome segregation is dependent on crossovers (COs), which enable pairs of homologous chromosomes to segregate to opposite poles at meiosis I. In mammals, the majority of meiotic chromosome segregation errors result from a lack of COs between homologs. Observations in Homo sapiens and Drosophila melanogaster have revealed a second class of exceptional events in which a CO occurred near the centromere of the missegregated chromosome. We show that in wild-type strains of Saccharomyces cerevisiae, most spore inviability is due to precocious separation of sister chromatids (PSSC) and that PSSC is often associated with centromere-proximal crossing over. COs, as opposed to nonreciprocal recombination events (NCOs), are preferentially associated with missegregation. Strains mutant for the RecQ homolog, SGS1, display reduced spore viability and increased crossing over. Much of the spore inviability in sgs1 results from PSSC, and these events are often associated with centromere-proximal COs, just as in wild type. When crossing over in sgs1 is reduced by the introduction of a nonnull allele of SPO11, spore viability is improved, suggesting that the increased PSSC is due to increased crossing over. We present a model for PSSC in which a centromere-proximal CO promotes local loss of sister-chromatid cohesion.

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