Analysis of DNA double-strand break repair pathways in mice
Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis , Volume 614 - Issue 1-2 p. 95- 108
During the last years significant new insights have been gained into the mechanism and biological relevance of DNA double-strand break (DSB) repair in relation to genome stability. DSBs are a highly toxic DNA lesion, because they can lead to chromosome fragmentation, loss and translocations, eventually resulting in cancer. DSBs can be induced by cellular processes such as V(D)J recombination or DNA replication. They can also be introduced by exogenous agents DNA damaging agents such as ionizing radiation or mitomycin C. During evolution several pathways have evolved for the repair of these DSBs. The most important DSB repair mechanisms in mammalian cells are nonhomologous end-joining and homologous recombination. By using an undamaged repair template, homologous recombination ensures accurate DSB repair, whereas the untemplated nonhomologous end-joining pathway does not. Although both pathways are active in mammals, the relative contribution of the two repair pathways to genome stability differs in the different cell types. Given the potential differences in repair fidelity, it is of interest to determine the relative contribution of homologous recombination and nonhomologous end-joining to DSB repair. In this review, we focus on the biological relevance of DSB repair in mammalian cells and the potential overlap between nonhomologous end-joining and homologous recombination in different tissues.
|Cell survival, DNA double-strand breaks, Embryonic stem cells, Homologous recombination, Ionizing radiation, Mouse embryonic fibroblasts, Nonhomologous end-joining|
|Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis|
|Organisation||Erasmus MC: University Medical Center Rotterdam|
Brugmans, L.J.L, Kanaar, R, & Essers, J. (2007). Analysis of DNA double-strand break repair pathways in mice. Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 614(1-2), 95–108. doi:10.1016/j.mrfmmm.2006.01.022