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Genetics, Vol. 168, 2067-2076, December 2004, Copyright © 2004
doi:10.1534/genetics.104.033902
End-Joining Repair of Double-Strand Breaks in Drosophila melanogaster Is Largely DNA Ligase IV Independent
Mitch McVey*,
,1,
Dora Radut* and
Jeff J. Sekelsky*,
* Department of Biology, University of North Carolina, Chapel Hill, North Carolina 27599
SPIRE Program, University of North Carolina, Chapel Hill, North Carolina 27599
Program in Molecular Biology and Biotechnology, University of North Carolina, Chapel Hill, North Carolina 27599
1 Corresponding author: Department of Biology, CB 3280, 303 Fordham Hall, University of North Carolina, Chapel Hill, NC 27599-3280.
E-mail: mmcvey{at}email.unc.edu
Repair of DNA double-strand breaks can occur by either nonhomologous end joining or homologous recombination. Most nonhomologous end joining requires a specialized ligase, DNA ligase IV (Lig4). In Drosophila melanogaster, double-strand breaks created by excision of a P element are usually repaired by a homologous recombination pathway called synthesis-dependent strand annealing (SDSA). SDSA requires strand invasion mediated by DmRad51, the product of the spn-A gene. In spn-A mutants, repair proceeds through a nonconservative pathway involving the annealing of microhomologies found within the 17-nt overhangs produced by P excision. We report here that end joining of P-element breaks in the absence of DmRad51 does not require Drosophila LIG4. In wild-type flies, SDSA is sometimes incomplete, and repair is finished by an end-joining pathway that also appears to be independent of LIG4. Loss of LIG4 does not increase sensitivity to ionizing radiation in late-stage larvae, but lig4 spn-A double mutants do show heightened sensitivity relative to spn-A single mutants. Together, our results suggest that a LIG4-independent end-joining pathway is responsible for the majority of double-strand break repair in the absence of homologous recombination in flies.
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