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Originally published as Genetics Published Articles Ahead of Print on June 11, 2007.
Genetics, Vol. 176, 2027-2033, August 2007, Copyright © 2007
doi:10.1534/genetics.107.076968
Synapsis-Defective Mutants Reveal a Correlation Between Chromosome Conformation and the Mode of Double-Strand Break Repair During Caenorhabditis elegans Meiosis
Sarit Smolikov*,
Andreas Eizinger*,
Allison Hurlburt*,
Eric Rogers*,
Anne M. Villeneuve
and
Mónica P. Colaiácovo*,1
* Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115 and Departments of Developmental Biology and Genetics, Stanford University School of Medicine, Stanford, California 94305
1 Corresponding author: Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, NRB-334, Boston, MA 02115.
E-mail: mcolaiacovo{at}genetics.med.harvard.edu
SYP-3 is a new structural component of the synaptonemal complex (SC) required for the regulation of chromosome synapsis. Both chromosome morphogenesis and nuclear organization are altered throughout the germlines of syp-3 mutants. Here, our analysis of syp-3 mutants provides insights into the relationship between chromosome conformation and the repair of meiotic double-strand breaks (DSBs). Although crossover recombination is severely reduced in syp-3 mutants, the production of viable offspring accompanied by the disappearance of RAD-51 foci suggests that DSBs are being repaired in these synapsis-defective mutants. Our studies indicate that once interhomolog recombination is impaired, both intersister recombination and nonhomologous end-joining pathways may contribute to repair during germline meiosis. Moreover, our studies suggest that the conformation of chromosomes may influence the mode of DSB repair employed during meiosis.
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Genetics 2007 176: NP.
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