沃纳综合征解旋酶对复制叉与霍利迪连接体之间重复结构转变的主动控制。
Active Control of Repetitive Structural Transitions between Replication Forks and Holliday Junctions by Werner Syndrome Helicase.
作者信息
Shin Soochul, Lee Jinwoo, Yoo Sangwoon, Kulikowicz Tomasz, Bohr Vilhelm A, Ahn Byungchan, Hohng Sungchul
机构信息
Department of Physics and Astronomy, Seoul National University, Seoul 08826, Republic of Korea; Institute of Applied Physics, Seoul National University, Seoul 08826, Republic of Korea; National Center for Creative Research Initiatives, Seoul National University, Seoul 08826, Republic of Korea.
Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
出版信息
Structure. 2016 Aug 2;24(8):1292-1300. doi: 10.1016/j.str.2016.06.004. Epub 2016 Jul 14.
The reactivation of stalled DNA replication via fork regression invokes Holliday junction formation, branch migration, and the recovery of the replication fork after DNA repair or error-free DNA synthesis. The coordination mechanism for these DNA structural transitions by molecular motors, however, remains unclear. Here we perform single-molecule fluorescence experiments with Werner syndrome protein (WRN) and model replication forks. The Holliday junction is readily formed once the lagging arm is unwound, and migrated unidirectionally with 3.2 ± 0.03 bases/s velocity. The recovery of the replication fork was controlled by branch migration reversal of WRN, resulting in repetitive fork regression. The Holliday junction formation, branch migration, and migration direction reversal are all ATP dependent, revealing that WRN uses the energy of ATP hydrolysis to actively coordinate the structural transitions of DNA.
通过叉回归重新激活停滞的DNA复制会引发霍利迪连接的形成、分支迁移以及DNA修复或无错DNA合成后复制叉的恢复。然而，分子马达对这些DNA结构转变的协调机制仍不清楚。在这里，我们用沃纳综合征蛋白（WRN）和模型复制叉进行了单分子荧光实验。一旦滞后臂解开，霍利迪连接很容易形成，并以3.2±0.03个碱基/秒的速度单向迁移。复制叉的恢复由WRN的分支迁移逆转控制，导致重复的叉回归。霍利迪连接的形成、分支迁移和迁移方向逆转均依赖于ATP，这表明WRN利用ATP水解的能量来积极协调DNA的结构转变。
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