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GENES & DEVELOPMENT 19:863-874, 2005
©2005 by Cold Spring Harbor Laboratory Press; ISSN 0890-9369/ $5.00
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RESEARCH PAPER

Multiple branches of the meiotic recombination pathway contribute independently to homolog pairing and stable juxtaposition during meiosis in budding yeast

Tamara L. Peoples-Holst1,2 and Sean M. Burgess1,2,3,4

1 Section of Molecular and Cellular Biology, 2 Biochemistry and Molecular Biology Graduate Group, and 3 Center for Genetics and Development, University of California, Davis, Davis, California 95616, USA

A unique aspect of meiosis is the segregation of homologous chromosomes at the meiosis I division. Homologs are physically connected prior to segregation by crossing over between nonsister chromatids. Crossovers arise from the repair of induced double-strand breaks (DSBs). In many organisms, more DSBs are formed than crossovers in a given nucleus. It has been previously suggested that repair of DSBs to noncrossover recombination products aids homolog alignment. Here we explore how two modes of the meiotic recombination pathway (crossover and noncrossover) and meiotic telomere reorganization contribute to the pairing and close juxtaposition of homologous chromosomes in budding yeast. We found that intermediates in the DSB repair pathway leading to both crossover and noncrossover recombination products contribute independently to close, stable homolog juxtaposition (CSHJ), a measurable state of homolog pairing. Analysis of the ndj1{Delta} mutant indicates that the effect of meiotic telomere reorganization on CSHJ is exerted through recombination intermediates at interstitial chromosomal loci, perhaps through the noncrossover branch of the DSB repair pathway. We suggest that transient, early DSB-initiated interactions, including those that give rise to noncrossovers, are important for homolog recognition and juxtaposition.

[Keywords: Homolog; meiosis; pairing; recombination; telomeres]

Received December 28, 2004; revised version accepted February 15, 2005.


Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.1293605.

4 Corresponding author.

E-MAIL smburgess{at}ucdavis.edu; FAX (530) 752-3085.


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