Werner syndrome protein, the MRE11 complex and ATR: menage-à-trois in guarding genome stability during DNA replication?
Werner syndrome protein, the MRE11 complex and ATR: menage-à-trois in guarding genome stability during DNA replication?
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DOI：
10.1002/bies.10411
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发表时间：
2004-03
期刊：
影响因子：
--
通讯作者：
P. Pichierri;A. Franchitto
中科院分区：
文献类型：
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作者：
P. Pichierri;A. Franchitto
DNA复制过程的正确执行对于维持细胞的基因组完整性至关重要。几种类型的来源，内源性和外源性，可以引起DNA损伤，导致DNA复制叉停滞。检查点传感器感知复制阻塞的过程以及如何激活导致停滞分叉的解决方案的途径仍然没有完全理解。然而，最近出现的证据表明，一个候选人的传感器的复制压力是ATR，并与RecQ家族解旋酶的成员，沃纳综合征蛋白（WRN）和MRE 11复合物，可以合作，以促进重新启动的DNA合成，通过解决停滞的复制叉。在这里，我们讨论了WRN，MRE11复合物和ATR激酶如何共同作用，以应对复制阻断，以避免DNA复制叉崩溃和基因组不稳定。
The correct execution of the DNA replication process is crucially import for the maintenance of genome integrity of the cell. Several types of sources, both endogenous and exogenous, can give rise to DNA damage leading to the DNA replication fork arrest. The processes by which replication blockage is sensed by checkpoint sensors and how the pathway leading to resolution of stalled forks is activated are still not completely understood. However, recent emerging evidence suggests that one candidate for a sensor of replication stress is ATR and that, together with a member of RecQ family helicases, Werner syndrome protein (WRN) and MRE11 complex, can collaborate to promote the restarting of DNA synthesis through the resolution of stalled replication forks. Here, we discuss how WRN, the MRE11 complex and the ATR kinase could work together in response to replication blockage to avoid DNA replication fork collapse and genome instability.