Kadyrov Farid A, Drake John W
Laboratory of Molecular Genetics, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709-2233, USA.
J Biol Chem. 2004 Aug 20;279(34):35735-40. doi: 10.1074/jbc.M403942200. Epub 2004 Jun 11.
The rescue of stalled replication forks via a series of steps that include fork regression, template switching, and fork restoration often has been proposed as a major mechanism for accurately bypassing non-coding DNA lesions. Bacteriophage T4 encodes almost all of the proteins required for its own DNA replication, recombination, and repair. Both recombination and recombination repair in T4 rely on UvsX, a RecA-like recombinase. We show here that UvsX plus the T4-encoded helicase Dda suffice to rescue stalled T4 replication forks in vitro. This rescue is based on two sequential template-switching reactions that allow DNA replication to bypass a non-coding DNA lesion in a non-mutagenic manner.
通过一系列步骤(包括叉回归、模板切换和叉修复)来拯救停滞的复制叉,通常被认为是准确绕过非编码DNA损伤的主要机制。噬菌体T4编码其自身DNA复制、重组和修复所需的几乎所有蛋白质。T4中的重组和重组修复都依赖于UvsX,一种RecA样重组酶。我们在此表明,UvsX加上T4编码的解旋酶Dda足以在体外拯救停滞的T4复制叉。这种拯救基于两个连续的模板切换反应,使DNA复制能够以非诱变方式绕过非编码DNA损伤。