Rescuing Stalled or Damaged Replication Forks
Rescuing Stalled or Damaged Replication Forks
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DOI：
10.1101/cshperspect.a012815
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发表时间：
2013-05-01
影响因子：
7.2
通讯作者：
Pasero, Philippe
中科院分区：
文献类型：
--
作者：
Yeeles, Joseph T. P.;Poli, Jerome;Pasero, Philippe
近年来，越来越多的研究表明，原核生物和真核生物具有复杂的机制来重新启动停滞或崩溃的复制分叉。虽然这些过程在细菌中得到了更好的理解，但在解释真核细胞中叉子重启机制如何运作方面也取得了重大突破。特别是，在前导链和分叉回归上的重述现在被确定为两个系统中停滞分叉的维护和恢复的关键。尽管所涉及的因素之间缺乏守恒，但这些机制在真核生物和原核生物中惊人地相似。然而，它们的不同之处在于，在真核生物中，分叉重启发生在染色质的背景下，并受到多种调控途径的控制。
In recent years, an increasing number of studies have shown that prokaryotes and eukaryotes are armed with sophisticated mechanisms to restart stalled or collapsed replication forks. Although these processes are better understood in bacteria, major breakthroughs have also been made to explain how fork restart mechanisms operate in eukaryotic cells. In particular, repriming on the leading strand and fork regression are now established as critical for the maintenance and recovery of stalled forks in both systems. Despite the lack of conservation between the factors involved, these mechanisms are strikingly similar in eukaryotes and prokaryotes. However, they differ in that fork restart occurs in the context of chromatin in eukaryotes and is controlled by multiple regulatory pathways.