ArticleGenetics2005
Lig4 and rad54 are required for repair of DNA double-strand breaks induced by P-element excision in Drosophila.
Article in Genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
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- A fly model establishes distinct mechanisms for synthetic CRISPR/Cas9 sex distorters.PLoS genetics · 2020Article
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- Females and males contribute in opposite ways to the evolution of gene order in Drosophila.PloS one · 2013Article
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- Efficient gene targeting in Drosophila by direct embryo injection with zinc-finger nucleases.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
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- Multiple-pathway analysis of double-strand break repair mutations in Drosophila.PLoS genetics · 2007Article
- Drosophila ATR in double-strand break repair.Genetics · 2007Article
- Targeted engineering of the Caenorhabditis elegans genome following Mos1-triggered chromosomal breaks.The EMBO journal · 2007Article
- Drosophila mus301/spindle-C encodes a helicase with an essential role in double-strand DNA break repair and meiotic progression.Genetics · 2006Article
- Differential usage of alternative pathways of double-strand break repair in Drosophila.Genetics · 2006Article
- ATP-dependent chromatin remodeling complexes in Drosophila.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2006Review
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- An optimized TALEN application for mutagenesis and screening inCellular logisticsArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Site-specific double-strand breaks (DSBs) were generated in the white gene located on the X chromosome of Drosophila by excision of the w(hd) P-element. To investigate the role of nonhomologous end joining (NHEJ) and homologous recombination (HR) in the repair of these breaks, the w(hd) 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 w(hd) 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.
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