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Originally published as Genetics Published Articles Ahead of Print on March 4, 2007.
Genetics, Vol. 176, 63-72, May 2007, Copyright © 2007
doi:10.1534/genetics.107.070557
Heteroduplex DNA in Meiotic Recombination in Drosophila mei-9 Mutants
Sarah J. Radford*,
Susan McMahan
,
Hunter L. Blanton*,1 and
Jeff Sekelsky*,,2
* Curriculum in Genetics and Molecular Biology and Department of Biology, University of North Carolina, Chapel Hill, North Carolina 27599
2 Corresponding author: Department of Biology, CB 3280, 303 Fordham Hall, University of North Carolina, Chapel Hill, NC 27599-3280.
E-mail: sekelsky{at}unc.edu
Meiotic recombination gives rise to crossovers, which are required in most organisms for the faithful segregation of homologous chromosomes during meiotic cell division. Characterization of crossover-defective mutants has contributed much to our understanding of the molecular mechanism of crossover formation. We report here a molecular analysis of recombination in a Drosophila melanogaster crossover-defective mutant, mei-9. In the absence of mei-9 activity, postmeiotic segregation associated with noncrossovers occurs at the expense of crossover products, suggesting that the underlying meiotic function for MEI-9 is in crossover formation rather than mismatch repair. In support of this, analysis of the arrangement of heteroduplex DNA in the postmeiotic segregation products reveals different patterns from those observed in Drosophila Msh6 mutants, which are mismatch-repair defective. This analysis also provides evidence that the double-strand break repair model applies to meiotic recombination in Drosophila. Our results support a model in which MEI-9 nicks Holliday junctions to generate crossovers during meiotic recombination, and, in the absence of MEI-9 activity, the double Holliday junction intermediate instead undergoes dissolution to generate noncrossover products in which heteroduplex is unrepaired.
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