Crossover interference is abolished in the absence of a synaptonemal complex protein.
In the zip1 mutant, meiotic chromosomes fail to synapse, owing to the absence of a structural component of the synaptonemal complex (SC). This mutant has been analyzed for the ability to carry out several functions that have been proposed for the SC. The data presented show that the zip1 mutation does not affect chiasma function and confers only modest defects in meiotic recombination and sister chromatid cohesion. In contrast, crossover interference is completely abolished in the absence of Zip1. These data are the first to establish a molecular link between cytological observations of the SC and the genetic phenomenon of interference.
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Department of Biology, Yale University, New Haven, Connecticut 06520-8103.
Roeder
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D002875:Chromosomes / Q000502:physiology*; D003434:Crossing Over, Genetic; D005656:Fungal Proteins / Q000502:physiology*; D005785:Gene Conversion; D008540:Meiosis; D009687:Nuclear Proteins; D011995:Recombination, Genetic; D012441:Saccharomyces cerevisiae / Q000235:genetics*; D029701:Saccharomyces cerevisiae Proteins; D013172:Spores, Fungal; D013573:Synaptonemal Complex / Q000502:physiology*
D005656:Fungal Proteins; D009687:Nuclear Proteins; D029701:Saccharomyces cerevisiae Proteins; C090118:Zip1 protein, S cerevisiae