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doi:10.1534/genetics.106.067330
A more recent version of this article appeared on March 1, 2007.
REGULAR RESEARCH PAPERS |
Drosophila ATR in double-strand break repair
Jeannine R LaRocque 1, Burnley R Jaklevic 2, Tin Tin Su 2 and Jeff Sekelsky 1*
1 University of North Carolina-Chapel Hill
2 University of Colorado-Boulder
* To whom correspondence should be addressed. E-mail: sekelsky{at}unc.edu.
Submitted on October 26, 2006
Revised on December 14, 2006
Accepted on 20 December 2006
The ability of a cell to sense and respond to DNA damage is essential for genome stability. An important aspect of the response is arrest of the cell-cycle, presumably to allow time for repair. ATM and ATR are essential for such cell cycle control, but some observations suggest that they also play a direct role in DNA repair. The Drosophila ortholog of ATR, MEI-41, mediates the DNA damage-dependent G2-M checkpoint. We examined the role of MEI-41 in repair of double-strand breaks (DSBs) induced by P element excision. We found that mei-41 mutants are defective in completing the later steps of homologous recombination repair, but have no defects in end-joining repair. We hypothesized that these repair defects are the result of loss of checkpoint control. To test this, we genetically reduced mitotic cyclin levels and also examined repair in grp (DmChk1) and lok (DmChk2) mutants. Our results suggest that a significant component of the repair defects is due to loss of MEI 41-dependent cell cycle regulation. However, this does not account for all of the defects we observed. We propose a novel role for MEI-41 in DSB repair, independent of the Chk1/Chk2-mediated checkpoint response.
Key Words: DNA repair, Double-strand breaks, Drosophila, checkpoints
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