Manna A C, Pai K S, Bussiere D E, Davies C, White S W, Bastia D
Department of Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Cell. 1996 Nov 29;87(5):881-91. doi: 10.1016/s0092-8674(00)81995-9.
Termination of DNA replication at a sequence-specific replication terminus is potentiated by the binding of the replication terminator protein (RTP) to the terminus sequence, causing polar arrest of the replicative helicase (contrahelicase activity). Two alternative models have been proposed to explain the mechanism of replication fork arrest. In the first model, the RTP-terminus DNA interaction simply imposes a polar barrier to helicase movement without involving any specific interaction between the helicase and the terminator proteins. The second model proposes that there is a specific interaction between the two proteins, and that the DNA-protein interaction both restricts the fork arrest to the replication terminus and determines the polarity of the process. The evidence presented in this paper strongly supports the second model.
DNA复制在特定序列的复制终点处终止,这一过程因复制终止蛋白(RTP)与终点序列的结合而得到增强,从而导致复制性解旋酶的极性停滞(反解旋酶活性)。人们提出了两种不同的模型来解释复制叉停滞的机制。在第一个模型中,RTP-终点DNA相互作用仅仅对解旋酶的移动施加了一个极性屏障,而不涉及解旋酶与终止蛋白之间的任何特定相互作用。第二个模型提出,这两种蛋白质之间存在特定相互作用,并且DNA-蛋白质相互作用既将叉停滞限制在复制终点,又决定了这一过程的极性。本文提供的证据有力地支持了第二个模型。