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Originally published as Genetics Published Articles Ahead of Print on April 15, 2007.
Genetics, Vol. 176, 773-787, June 2007, Copyright © 2007
doi:10.1534/genetics.107.071100
A Novel Nonnull ZIP1 Allele Triggers Meiotic Arrest With Synapsed Chromosomes in Saccharomyces cerevisiae
Neal Mitra* and
G. Shirleen Roeder*,
,
,1
* Department of Molecular, Cellular and Developmental Biology, Howard Hughes Medical Institute and Department of Genetics, Yale University, New Haven, Connecticut 06520-8103
1 Corresponding author: Department of Molecular, Cellular and Developmental Biology, Yale University, P.O. Box 208103, New Haven, CT 06520-8103.
E-mail: shirleen.roeder{at}yale.edu
During meiotic prophase, assembly of the synaptonemal complex (SC) brings homologous chromosomes into close apposition along their lengths. The Zip1 protein is a major building block of the SC in Saccharomyces cerevisiae. In the absence of Zip1, SC fails to form, cells arrest or delay in meiotic prophase (depending on strain background), and crossing over is reduced. We created a novel allele of ZIP1, zip1-4LA, in which four leucine residues in the central coiled-coil domain have been replaced by alanines. In the zip1-4LA mutant, apparently normal SC assembles with wild-type kinetics; however, crossing over is delayed and decreased compared to wild type. The zip1-4LA mutant undergoes strong checkpoint-induced arrest in meiotic prophase; the defect in cell cycle progression is even more severe than that of the zip1 null mutant. When the zip1-4LA mutation is combined with the pch2 checkpoint mutation, cells sporulate with wild-type efficiency and crossing over occurs at wild-type levels. This result suggests that the zip1-4LA defect in recombination is an indirect consequence of cell cycle arrest. Previous studies have suggested that the Pch2 protein acts in a checkpoint pathway that monitors chromosome synapsis. We hypothesize that the zip1-4LA mutant assembles aberrant SC that triggers the synapsis checkpoint.
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Genetics 2007 176: NP.
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