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Genetics, Vol. 163, 1273-1286, April 2003, Copyright © 2003

Crossover Interference in Saccharomyces cerevisiae Requires a TID1/RDH54- and DMC1-Dependent Pathway

Miki Shinoharaa,b, Kazuko Sakaib, Akira Shinoharaa,b,c, and Douglas K. Bishopa
a Department of Radiation and Cellular Oncology and Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, Illinois 60637,
b Department of Biology, Graduate School of Science, Osaka University, Toyonaka, Osaka 560-0043, Japan
c Precursory Research for Embryonic Science and Technology, Japanese Science and Technology, Toyonaka, Osaka 560-0043, Japan

Corresponding author: Douglas K. Bishop, Cummings Life Science Center, 920 E. 58th St., Chicago, IL 60637., dbishop{at}midway.uchicago.edu (E-mail)

Communicating editor: L. S. SYMINGTON

Two RecA-like recombinases, Rad51 and Dmc1, function together during double-strand break (DSB)-mediated meiotic recombination to promote homologous strand invasion in the budding yeast Saccharomyces cerevisiae. Two partially redundant proteins, Rad54 and Tid1/Rdh54, act as recombinase accessory factors. Here, tetrad analysis shows that mutants lacking Tid1 form four-viable-spore tetrads with levels of interhomolog crossover (CO) and noncrossover recombination similar to, or slightly greater than, those in wild type. Importantly, tid1 mutants show a marked defect in crossover interference, a mechanism that distributes crossover events nonrandomly along chromosomes during meiosis. Previous work showed that dmc1{Delta} mutants are strongly defective in strand invasion and meiotic progression and that these defects can be partially suppressed by increasing the copy number of RAD54. Tetrad analysis is used to show that meiotic recombination in RAD54-suppressed dmc1{Delta} cells is similar to that in tid1; the frequency of COs and gene conversions is near normal, but crossover interference is defective. These results support the proposal that crossover interference acts at the strand invasion stage of recombination.




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