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Pds5 is required for homologue pairing and inhibits synapsis of sister chromatids during yeast meiosis

¹ Department of Biological Science, The Florida State University, Tallahassee, FL 32306
² Department of Embryology, Carnegie Institution of Washington, Baltimore, MD 21218

Correspondence to Hong-Guo Yu: hyu{at}bio.fsu.edu

During meiosis, homologues become juxtaposed and synapsed along their entire length. Mutations in the cohesin complex disrupt not only sister chromatid cohesion but also homologue pairing and synaptonemal complex formation. In this study, we report that Pds5, a cohesin-associated protein known to regulate sister chromatid cohesion, is required for homologue pairing and synapsis in budding yeast. Pds5 colocalizes with cohesin along the length of meiotic chromosomes. In the absence of Pds5, the meiotic cohesin subunit Rec8 remains bound to chromosomes with only minor defects in sister chromatid cohesion, but sister chromatids synapse instead of homologues. Double-strand breaks (DSBs) are formed but are not repaired efficiently. In addition, meiotic chromosomes undergo hypercondensation. When the mitotic cohesin subunit Mcd1 is substituted for Rec8 in Pds5-depleted cells, chromosomes still hypercondense, but synapsis of sister chromatids is abolished. These data suggest that Pds5 modulates the Rec8 activity to facilitate chromosome morphological changes required for homologue synapsis, DSB repair, and meiotic chromosome segregation.

Abbreviations used in this paper: CE, central element; ChIP, chromatin immunoprecipitation; DSB, double-strand break; LE, lateral element; SC, synaptonemal complex.

© 2009 Jin et al.
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This article has been cited by other articles:

• Leslie, M. (2009). Stopping sister synapses. JCB 186: 632-632 [Full Text]  

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