Li Dawei, Lv Bei, Zhang Hao, Lee Jasmine Yiqin, Li Tianhu
Key Lab of Forest Genetics and Biotechnology, Nanjing Forestry University, 159 Longpan Road, Nanjing 210037, China; Division of Chemistry and Biological Chemistry, Nanyang Technological University, 21 Nanyang Link, 637371 Singapore, Singapore.
Division of Chemistry and Biological Chemistry, Nanyang Technological University, 21 Nanyang Link, 637371 Singapore, Singapore.
Bioorg Med Chem Lett. 2015 Apr 15;25(8):1709-1714. doi: 10.1016/j.bmcl.2015.02.070. Epub 2015 Mar 7.
Unlike chemical damages on DNA, physical alterations of B-form of DNA occur commonly in organisms that serve as signals for specified cellular events. Although the modes of action for repairing of chemically damaged DNA have been well studied nowadays, the repairing mechanisms for physically altered DNA structures have not yet been understood. Our current in vitro studies show that both breakdown of stable non-B DNA structures and resumption of canonical B-conformation of DNA can take place during the courses of isothermal helicase-dependent amplification (HDA). The pathway that makes the non-B DNA structures repairable is presumably the relieving of the accumulated torsional stress that was caused by the positive supercoiling. Our new findings suggest that living organisms might have evolved this distinct and economical pathway for repairing their physically altered DNA structures.
与DNA的化学损伤不同，DNA B型的物理改变在作为特定细胞事件信号的生物体中普遍存在。尽管如今对化学损伤DNA的修复作用模式已进行了充分研究，但对物理改变的DNA结构的修复机制仍未了解。我们目前的体外研究表明，在等温解旋酶依赖性扩增（HDA）过程中，稳定的非B型DNA结构的破坏和DNA经典B型构象的恢复均可发生。使非B型DNA结构可修复的途径大概是缓解由正超螺旋引起的累积扭转应力。我们的新发现表明，生物体可能已经进化出这种独特且经济的途径来修复其物理改变的DNA结构。
