A fork-clearing role for UvrD
A fork-clearing role for UvrD
复制标题
DOI：
10.1111/j.1365-2958.2005.04753.x
复制
发表时间：
2005-09-01
影响因子：
3.6
通讯作者：
Michel, B
中科院分区：
文献类型：
--
作者：
Florés, MJ;Sanchez, N;Michel, B
复制蛋白的失活导致复制机制的分解，并产生复制重新激活的需要。在几个复制突变体中，在叉被异构化为四臂连接后发生重新启动，这种反应称为复制叉逆转。修复解旋酶UvrD对于大肠杆菌聚合酶III的聚合酶（DnaE）或β-钳（DnaN）亚基失活后的复制叉逆转以及半容许温度下dnaEts和dnaNts突变体的活力至关重要。我们在这里表明，recA、recFOR、recJ或recQ重组基因的失活抑制了复制叉逆转对UvrD的需求，并抑制了在半允许温度下uvrD失活对Pol IIIts突变体赋予的致命性。我们提出RecA以RecQ-RecJ-RecFOR依赖的方式不适当地结合到dnaEts和dnaNts突变体中被阻断的复制叉，并且UvrD通过去除RecA或RecA制造的结构来起作用，从而允许复制叉逆转。因此，这项工作揭示了RecA绑定到阻塞的复制叉的无效反应的存在，这需要UvrD的动作来清除叉和正确的复制重新启动。
The inactivation of a replication protein causes the disassembly of the replication machinery and creates a need for replication reactivation. In several replication mutants, restart occurs after the fork has been isomerized into a four-armed junction, a reaction called replication fork reversal. The repair helicase UvrD is essential for replication fork reversal upon inactivation of the polymerase (DnaE) or the beta-clamp (DnaN) subunits of the Escherichia coli polymerase III, and for the viability of dnaEts and dnaNts mutants at semi-permissive temperature. We show here that the inactivation of recA, recFOR, recJ or recQ recombination genes suppresses the requirement for UvrD for replication fork reversal and suppresses the lethality conferred by uvrD inactivation to Pol IIIts mutants at semi-permissive temperature. We propose that RecA binds inappropriately to blocked replication forks in the dnaEts and dnaNts mutants in a RecQ- RecJ- RecFOR-dependent way and that UvrD acts by removing RecA or a RecA-made structure, allowing replication fork reversal. This work thus reveals the existence of a futile reaction of RecA binding to blocked replication forks, that requires the action of UvrD for fork-clearing and proper replication restart.