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Meiotic crossover number and distribution are regulated by a dosage compensation protein that resembles a condensin subunit

Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, California 97420, USA

Biological processes that function chromosome-wide are not well understood. Here, we show that the Caenorhabditis elegans protein DPY-28 controls two such processes, X-chromosome dosage compensation in somatic cells and meiotic crossover number and distribution in germ cells. DPY-28 resembles a subunit of condensin, a conserved complex required for chromosome compaction and segregation. In the soma, DPY-28 associates with the dosage compensation complex on hermaphrodite X chromosomes to repress transcript levels. In the germline, DPY-28 restricts crossovers. In many organisms, one crossover decreases the likelihood of another crossover nearby, an enigmatic process called crossover interference. In C. elegans, interference is complete: Only one crossover occurs per homolog pair. dpy-28 mutations increase crossovers, disrupt crossover interference, and alter crossover distribution. Early recombination intermediates (RAD-51 foci) increase concomitantly, suggesting that DPY-28 acts to limit double-strand breaks (DSBs). Reinforcing this view, dpy-28 mutations partially restore DSBs in mutants lacking HIM-17, a chromatin-associated protein required for DSB formation. Our work further links dosage compensation to condensin and establishes a new role for condensin components in regulating crossover number and distribution. We propose that both processes utilize a related mechanism involving changes in higher-order chromosome structure to achieve chromosome-wide effects.

[Keywords: X-chromosome dosage compensation; condensin; meiosis; crossover interference; epigenetics; DPY-28]]

Received September 24, 2007; revised version accepted November 15, 2007.

² Present address: Department of Medicine and Department of Biochemistry, Stanford University Medical Center, Stanford, CA 94305, USA;

³ Finnegan, Henderson, Farabow, Garrett and Dunner, L.L.P., Palo Alto, CA 94304, USA;

⁴ Department of Biology, University of Utah, Salt Lake City, UT 84112, USA;

⁵ Cell and Molecular Imaging Center, Department of Biology, San Francisco State University, San Francisco, CA 94132 USA

⁶ Corresponding author.

E-MAIL bjmeyer{at}berkeley.edu; FAX (510) 643-5584.

Supplemental material is available at http://www.genesdev.org.

Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.1618508

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