期刊
NUCLEIC ACIDS RESEARCH
卷 41, 期 16, 页码 7589-7605出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkt556
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资金
- Bundesministerium fur Bildung und Forschung [BMBF: 02NUK005C, 03NUK001B]
- Bundesministerium fur Wirtschaft und Technologie [BMWi: ESA-AO-08-IBER, 50WB1229]
- Bundesministerium fur Bildung und Forschung Germany
Although the DNA double-strand break (DSB) is defined as a rupture in the double-stranded DNA molecule that can occur without chemical modification in any of the constituent building blocks, it is recognized that this form is restricted to enzyme-induced DSBs. DSBs generated by physical or chemical agents can include at the break site a spectrum of base alterations (lesions). The nature and number of such chemical alterations define the complexity of the DSB and are considered putative determinants for repair pathway choice and the probability that errors will occur during this processing. As the pathways engaged in DSB processing show distinct and frequently inherent propensities for errors, pathway choice also defines the error-levels cells opt to accept. Here, we present a classification of DSBs on the basis of increasing complexity and discuss how complexity may affect processing, as well as how it may cause lethal or carcinogenic processing errors. By critically analyzing the characteristics of DSB repair pathways, we suggest that all repair pathways can in principle remove lesions clustering at the DSB but are likely to fail when they encounter clusters of DSBs that cause a local form of chromothripsis. In the same framework, we also analyze the rational of DSB repair pathway choice.
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