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doi:10.1534/genetics.104.033464
A more recent version of this article appeared on February 1, 2005.
REGULAR RESEARCH PAPERS |
Lig4 and Rad54 are required for repair of DNA double-strand breaks induced by P-element excision in Drosophila
Ron J. Romeijn 1, Marcin M. Gorski 1, Martijn A. van Schie 2, Jasprina N. Noordermeer 2, Leon H. Mullenders 1, Wouter Ferro 1 and Albert Pastink 1*
1 Department of Toxicogenetics, Leiden University Medical Center (LUMC)
2 Lab. of Developmental Neurobiology, Department of Molecular Cell Biology, LUMC
* To whom correspondence should be addressed. E-mail: a.pastink{at}lumc.nl.
Submitted on July 12, 2004
Revised on September 15, 2004
Accepted on 8 November 2004
Site-specific double-strand breaks (DSBs) were generated in the white gene located on the X chromosome of Drosophila by excision of the whd P-element. To investigate the role of non-homologous end-joining (NHEJ) and homologous recombination (HR) in the repair of these breaks, the whd P-element was mobilized in flies carrying mutant alleles of either lig4 or rad54. The survival of both lig4 and rad54 deficient males was reduced to 25% in comparison to the wild type, indicating that both NHEJ and HR are involved in the repair P-induced gaps in males. Survival of lig4 deficient females was not affected at all, implying that HR using the homologous chromosome as a template, can partially compensate for the impaired NHEJ pathway. In rad54 mutant females survival was reduced to 70% after whd excision. PCR analysis indicated that the undamaged homologous chromosome may compensate for the potential loss of the broken chromosome in rad54 mutant females after excision. Molecular analysis of the repair junctions revealed microhomology (2-8 bp) dependent DSB-repair in most products. In the absence of Lig4, the 8-bp target site duplication is used more frequently for repair. Our data indicate the presence of efficient alternative end-joining mechanisms, which partly depend on the presence of microhomology but do not require Lig4.
Key Words: DNA double-strand break repair, DNA ligase IV, Drosophila, P-element transposition, rad54
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