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MBC in Press, published online ahead of print October 12, 2005
Mol. Biol. Cell 10.1091/mbc.E05-05-0465

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Submitted on May 31, 2005
Revised on September 26, 2005
Accepted on September 29, 2005

Partner Choice during Meiosis Is Regulated by Hop1-promoted Dimerization of Mek1

Hengyao Niu,*{dagger} Lihong Wan,*{dagger} Bridget Baumgartner,{ddagger} Dana Schaefer,* Josef Loidl,{sect} and Nancy M. Hollingsworth*

*Department of Biochemistry and Cell Biology, State University of New York at Stony Brook, Stony Brook, NY 11794-5215; {ddagger}Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030; {sect}Department of Chromosome Research, University of Vienna, A-1030 Vienna, Austria

Monitoring Editor: Orna Cohen-Fix

Meiotic recombination differs from mitotic recombination in that DSBs are repaired using homologous chromosomes, rather than sister chromatids. This change in partner choice is due to a barrier to sister chromatid repair (BSCR) created by the meiosis-specific kinase, Mek1, in a complex with two other meiosis-specific proteins, Hop1 and Red1. HOP1 contains two functional domains, called the N and C domains. Analysis of a point mutation that specifically inactivates the C domain (hop1-K593A) reveals that the N domain is sufficient for Hop1 localization to chromosomes and for Red1 and Hop1 interactions. The C domain is needed for spore viability, chromosome synapsis and for preventing DMC1-independent DSB repair, indicating it plays a role in the BSCR. All of the hop1-K593A phenotypes can be bypassed by fusion of ectopic dimerization domains to Mek1, suggesting that the function of the C domain is to promote Mek1 dimerization. Hop1 is a DSB-dependent phosphoprotein whose phosphorylation requires the presence of the C domain, but is independent of MEK1. These results suggest a model in which Hop1 phosphorylation in response to DSBs triggers dimerization of Mek1 via the Hop1 C domain, thereby enabling Mek1 to phosphorylate target proteins that prevent repair of DSBs by sister chromatids.

{dagger}These authors contributed equally to this work.

Address correspondence to: Nancy M. Hollingsworth (nhollin{at}ms.cc.sunysb.edu)




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