Molecular mechanism of extreme DNA damage resistance in Deinococcus spp.

异常球菌属极端DNA损伤抵抗的分子机制。

• 批准号: 262034-2013
• 负责人: Junop, Murray
• 金额: $ 5.03万
• 依托单位: University of Western Ontario
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2016
• 资助国家: 加拿大
• 起止时间: 2016-01-01 至 2017-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=594710
• 关键词: Molecular; mechanism; extreme; DNA; damage

DNA Double-strand breaks represent the most lethal form of damage in the genome, resulting in genetic loss and/or chromosomal re-arrangement if not properly repaired. Sources of ionizing radiation (IR) responsible for such damage include cosmic radiation, radon and the decay of radioactive material left over from nuclear weapons testing and spent nuclear fuel generated during power production. Not surprisingly, tolerable levels of exposure to such ionizing radiation are exceedingly small for all forms of life. One notable exception is the bacterium Deinococcus radiodurans. Deinococcus is able to withstand a dose of ionizing radiation 1500 times greater than humans can survive and one that would obliterate the E. coli genome 10 times over [Battista 1997]. Remarkably, despite being shattered into hundreds of small DNA fragments, Deinococcus radiodurans readily reassembles a functional genome. This feat has been attributed to the combination of a number of protective mechanisms including the presence of multiple genome copies, characteristic genome structure, and known or novel DNA repair mechanisms. Although traditional repair mechanisms appear to be active in D. radiodurans, the speed and accuracy of repair displayed are inconsistent with all previously characterized pathways [Cox 2005].

DNA双链断裂是基因组中最致命的损伤形式，如果不正确修复，会导致遗传丢失和/或染色体重排。造成这种损害的电离辐射源包括宇宙辐射、氡和核武器试验遗留下来的放射性物质的衰变以及发电过程中产生的乏核燃料。毫不奇怪，对所有生命形式来说，暴露于这种电离辐射的可容忍水平都非常小。一个值得注意的例外是耐辐射异常球菌。异常球菌能够承受的电离辐射剂量是人类生存剂量的1500倍，这种剂量的辐射可以消灭大肠杆菌。大肠杆菌基因组的10倍[Battista 1997]。值得注意的是，尽管被粉碎成数百个小的DNA片段，但耐辐射奇球菌很容易重组功能基因组。这一壮举归因于许多保护机制的组合，包括多个基因组拷贝的存在，特征性基因组结构和已知或新的DNA修复机制。虽然传统的修复机制在D.对于耐放射性药物，显示的修复速度和准确性与所有先前表征的途径不一致[考克斯2005]。