ArticleMolecular and cellular biology1999
The Drosophila melanogaster DmRAD54 gene plays a crucial role in double-strand break repair after P-element excision and acts synergistically with Ku70 in the repair of X-ray damage.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 62 citations in OpenAlex.
- Genetic variation in P-element dysgenic sterility is associated with double-strand break repair and alternative splicing of TE transcripts.PLoS genetics · 2022Article
- Genetic mechanisms of formation of radiation-induced instability of the genome and its transgenerational effects in the descendants of chronically irradiated individuals of Drosophila melanogaster.Radiation and environmental biophysics · 2020Article
- Aging impairs double-strand break repair by homologous recombination in Drosophila germ cells.Aging cell · 2017Article
- The variant histone H2A.V of Drosophila--three roles, two guises.Chromosoma · 2013Review
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- Drosophila mus301/spindle-C encodes a helicase with an essential role in double-strand DNA break repair and meiotic progression.Genetics · 2006Article
- Regulation of homologous integration in yeast by the DNA repair proteins Ku70 and RecQ.Molecular genetics and genomics : MGG · 2005Article
- Lig4 and rad54 are required for repair of DNA double-strand breaks induced by P-element excision in Drosophila.Genetics · 2005Article
- Transcript profiling of Wilms tumors reveals connections to kidney morphogenesis and expression patterns associated with anaplasia.Oncogene · 2005Article
- Collaboration of homologous recombination and nonhomologous end-joining factors for the survival and integrity of mice and cells.Genes & development · 2004Article
- Relative contribution of DNA repair, cell cycle checkpoints, and cell death to survival after DNA damage in Drosophila larvae.Current biology : CB · 2004Article
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- Strand pairing by Rad54 and Rad51 is enhanced by chromatin.Genes & development · 2002Article
- DNA double-strand break-induced phosphorylation of Drosophila histone variant H2Av helps prevent radiation-induced apoptosis.Nucleic acids research · 2002Article
- Telomere length deregulation and enhanced sensitivity to genotoxic stress in Arabidopsis mutants deficient in Ku70.The EMBO journal · 2002Article
- DNA-dependent protein kinase suppresses double-strand break-induced and spontaneous homologous recombination.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Ku and the Stability of the Genome.Journal of biomedicine & biotechnology · 2002Article
- The role of DNA polymerase activity in human non-homologous end joining.Nucleic acids research · 2001Article
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The RAD54 gene has an essential role in the repair of double-strand breaks (DSBs) via homologous recombination in yeast as well as in higher eukaryotes. A Drosophila melanogaster strain deficient in the RAD54 homolog DmRAD54 is characterized by increased X-ray and methyl methanesulfonate (MMS) sensitivity. In addition, DmRAD54 is involved in the repair of DNA interstrand cross-links, as is shown here. However, whereas X-ray-induced loss-of-heterozygosity (LOH) events were completely absent in DmRAD54(-/-) flies, treatment with cross-linking agents or MMS resulted in only a slight reduction in LOH events in comparison with those in wild-type flies. To investigate the relative contributions of recombinational repair and nonhomologous end joining in DSB repair, a DmRad54(-/-)/DmKu70(-/-) double mutant was generated. Compared with both single mutants, a strong synergistic increase in X-ray sensitivity was observed in the double mutant. No similar increase in sensitivity was seen after treatment with MMS. Apparently, the two DSB repair pathways overlap much less in the repair of MMS-induced lesions than in that of X-ray-induced lesions. Excision of P transposable elements in Drosophila involves the formation of site-specific DSBs. In the absence of the DmRAD54 gene product, no male flies could be recovered after the excision of a single P element and the survival of females was reduced to 10% compared to that of wild-type flies. P-element excision involves the formation of two DSBs which have identical 3' overhangs of 17 nucleotides. The crucial role of homologous recombination in the repair of these DSBs may be related to the very specific nature of the breaks.
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