Lig4 and rad54 are required for repair of DNA double-strand breaks induced by P-element excision in Drosophila - PubMed (original) (raw)
Comparative Study
Lig4 and rad54 are required for repair of DNA double-strand breaks induced by P-element excision in Drosophila
Ron J Romeijn et al. Genetics. 2005 Feb.
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.
Figures
Figure 1.—
Structure and excision of the _whd P_-element. (A) The _whd P_-element is inserted into the sixth exon of the white locus on the X chromosome (O'H
are
and R
ubin
1983). The analysis of the repair junctions following the mobilization of the _whd P_-element was carried out using p7 and p9 primers (see
materials and methods
). (B) A DNA double-strand gap is generated after excision of the _whd P_-element by the _P_-element-specific endonuclease. This endonuclease is encoded by the P[_ry+_ Δ_2-3_](99B) _P_-element abbreviated here as Δ2-3. The endonucleolytic cleavage creates two staggered DSBs containing 17-bp 3′ overhangs within the 31-bp inverted repeats. TSD, target site duplication.
Figure 2.—
Scheme of the genetic crosses performed to mobilize the _whd P_-element. (A) To study the contribution of Lig4 to the repair of _whd P_-element-induced DSBs, y whd lig457/y whd lig457 females were crossed to y2 wa lig457/Y; Sb P[ry+ Δ_2-3_]/TM3, Ser males. In the next generation, both F1 males and females containing Δ2-3 transposase can be recognized on the basis of the Sb marker and were either directly analyzed by PCR and sequencing or mated to C(1)DX y w f females and M5 males, respectively. F2 males emerging from these crosses were analyzed as described for F1 progeny (see
materials and methods
). (B) The contribution of Rad54 to the repair of _P_-induced DSBs was studied by crossing y whd/y whd; JS17/SM5, Cy females to y2 wa/Y; A17-11/SM5, Cy; Sb P[ry+ Δ_2-3_]/TM3, Ser males. Both male and female F1 progenies containing Δ2-3 transposase were used for PCR and sequence analysis. In the control cross (not shown), y whd/y whd females were crossed to y2 wa; Sb P[ry+ Δ_2-3_]/TM3, Ser males and the offspring was analyzed as described above.
Figure 3.—
Mosaic eye phenotypes of _lig4-_proficient (middle) and _lig4_-mutant (right) females after the repair of _whd P_-element-induced DSBs. Use of the _wa_-containing chromosome as a template for recombination leads to restoration of the wild-type sequence of the white gene. Clonal outgrowth results in red (wild-type) spots against an apricot (wa) background. For comparison, the apricot eye of a wa, lig457 female not carrying the Δ2-3 transposase is shown on the left.
Similar articles
- The Drosophila melanogaster DNA Ligase IV gene plays a crucial role in the repair of radiation-induced DNA double-strand breaks and acts synergistically with Rad54.
Gorski MM, Eeken JC, de Jong AW, Klink I, Loos M, Romeijn RJ, van Veen BL, Mullenders LH, Ferro W, Pastink A. Gorski MM, et al. Genetics. 2003 Dec;165(4):1929-41. doi: 10.1093/genetics/165.4.1929. Genetics. 2003. PMID: 14704177 Free PMC article. - 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.
Kooistra R, Pastink A, Zonneveld JB, Lohman PH, Eeken JC. Kooistra R, et al. Mol Cell Biol. 1999 Sep;19(9):6269-75. doi: 10.1128/MCB.19.9.6269. Mol Cell Biol. 1999. PMID: 10454573 Free PMC article. - DNA ligase IV-deficient cells are more resistant to ionizing radiation in the absence of Ku70: Implications for DNA double-strand break repair.
Adachi N, Ishino T, Ishii Y, Takeda S, Koyama H. Adachi N, et al. Proc Natl Acad Sci U S A. 2001 Oct 9;98(21):12109-13. doi: 10.1073/pnas.201271098. Proc Natl Acad Sci U S A. 2001. PMID: 11593023 Free PMC article. - Mechanisms of DNA double strand break repair and chromosome aberration formation.
Iliakis G, Wang H, Perrault AR, Boecker W, Rosidi B, Windhofer F, Wu W, Guan J, Terzoudi G, Pantelias G. Iliakis G, et al. Cytogenet Genome Res. 2004;104(1-4):14-20. doi: 10.1159/000077461. Cytogenet Genome Res. 2004. PMID: 15162010 Review. - Microhomology-mediated end joining: Good, bad and ugly.
Seol JH, Shim EY, Lee SE. Seol JH, et al. Mutat Res. 2018 May;809:81-87. doi: 10.1016/j.mrfmmm.2017.07.002. Epub 2017 Jul 16. Mutat Res. 2018. PMID: 28754468 Free PMC article. Review.
Cited by
- Coordination between cell proliferation and apoptosis after DNA damage in Drosophila.
Ruiz-Losada M, González R, Peropadre A, Gil-Gálvez A, Tena JJ, Baonza A, Estella C. Ruiz-Losada M, et al. Cell Death Differ. 2022 Apr;29(4):832-845. doi: 10.1038/s41418-021-00898-6. Epub 2021 Nov 25. Cell Death Differ. 2022. PMID: 34824391 Free PMC article. - A fly model establishes distinct mechanisms for synthetic CRISPR/Cas9 sex distorters.
Fasulo B, Meccariello A, Morgan M, Borufka C, Papathanos PA, Windbichler N. Fasulo B, et al. PLoS Genet. 2020 Mar 13;16(3):e1008647. doi: 10.1371/journal.pgen.1008647. eCollection 2020 Mar. PLoS Genet. 2020. PMID: 32168334 Free PMC article. - An optimized TALEN application for mutagenesis and screening in Drosophila melanogaster.
Lee HB, Sebo ZL, Peng Y, Guo Y. Lee HB, et al. Cell Logist. 2015 Feb 27;5(1):e1023423. doi: 10.1080/21592799.2015.1023423. eCollection 2015 Jan-Mar. Cell Logist. 2015. PMID: 26196022 Free PMC article. - Contributions of DNA repair, cell cycle checkpoints and cell death to suppressing the DNA damage-induced tumorigenic behavior of Drosophila epithelial cells.
Dekanty A, Barrio L, Milán M. Dekanty A, et al. Oncogene. 2015 Feb 19;34(8):978-85. doi: 10.1038/onc.2014.42. Epub 2014 Mar 17. Oncogene. 2015. PMID: 24632609 - Females and males contribute in opposite ways to the evolution of gene order in Drosophila.
Díaz-Castillo C. Díaz-Castillo C. PLoS One. 2013 May 16;8(5):e64491. doi: 10.1371/journal.pone.0064491. Print 2013. PLoS One. 2013. PMID: 23696898 Free PMC article.
References
- Bingham, P. M., and B. H. Judd, 1981. A copy of the copia transposable element is very tightly linked to the Wa allele at the white locus of D. melanogaster. Cell 25: 705–711. - PubMed
- Bogue, M. A., C. Wang, C. Zhu and D. B. Roth, 1997. V(D)J recombination in Ku86-deficient mice: distinct effects on coding, signal, and hybrid joint formation. Immunity 7: 37–47. - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Molecular Biology Databases
Research Materials