Subdiffusion Supports Joining Of Correct Ends During Repair Of DNA Double-Strand Breaks

被引:35
作者
Girst, S. [1 ]
Hable, V. [1 ]
Drexler, G. A. [2 ]
Greubel, C. [1 ]
Siebenwirth, C. [1 ]
Haum, M. [1 ]
Friedl, A. A. [2 ]
Dollinger, G. [1 ]
机构
[1] Univ Bundeswehr Munchen, Angewandte Phys & Messtechn LRT2, D-85577 Neubiberg, Germany
[2] Univ Munich, Dept Radiat Oncol, D-80336 Munich, Germany
关键词
ANOMALOUS DIFFUSION; DYNAMICS; CELL; MOBILITY; PROTEINS; MOTION; SITES;
D O I
10.1038/srep02511
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];
摘要
The mobility of damaged chromatin regions in the nucleus may affect the probability of mis-repair. In this work, live-cell observation and distance tracking of GFP-tagged DNA damage response protein MDC1 was used to study the random-walk behaviour of chromatin domains containing radiation-induced DNA double-strand breaks (DSB). Our measurements indicate a subdiffusion-type random walk process with similar time dependence for isolated and clustered DSBs that were induced by 20 MeV proton or 43 MeV carbon ion micro-irradiation. As compared to normal diffusion, subdiffusion enhances the probability that both ends of a DSB meet, thus promoting high efficiency DNA repair. It also limits their probability of long-range movements and thus lowers the probability of mis-rejoining and chromosome aberrations.
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页数:6
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