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Fork regression is an active helicase-driven pathway in bacteriophage T4

机译:叉子消退是噬菌体T4中解旋酶驱动的活性途径

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Reactivation of stalled replication forks requires specialized mechanisms that can recognize the fork structure and promote downstream processing events. Fork regression has been implicated in several models of fork reactivation as a crucial processing step that supports repair. However, it has also been suggested that regressed forks represent pathological structures rather than physiological intermediates of repair. To investigate the biological role of fork regression in bacteriophage T4, we tested several mechanistic models of regression: strand exchangemediated extrusion, topology-driven fork reversal and helicase-mediated extrusion. Here, we report that UvsW, a T4 branch-specific helicase, is necessary for the accumulation of regressed forks in vivo, and that UvsW-catalysed regression is the dominant mechanism of origin-fork processing that contributes to double-strand end formation. We also show that UvsW resolves purified fork intermediates in vitro by fork regression. Regression is therefore part of an active, UvsW-driven pathway of fork processing in bacteriophage T4.
机译:重新激活已停止的复制叉需要特殊的机制,该机制可以识别叉结构并促进下游处理事件。货叉回归已涉及到货叉重新激活的多种模型中,这是支持修复的关键处理步骤。但是,也有人提出,退叉代表的是病理结构,而不是修复的生理学中间产物。为了研究叉子回归在噬菌体T4中的生物学作用,我们测试了几种回归机理模型:链交换介导的挤压,拓扑结构驱动的叉子反向和解旋酶介导的挤压。在这里,我们报告说,UvsW,T4分支特定的解旋酶,是体内降解叉的积累所必需的,并且UvsW催化的降解是原叉加工的主要机制,有助于双链末端的形成。我们还显示,UvsW通过fork回归在体外解析纯化的fork中间体。因此,回归是噬菌体T4中UvsW驱动的叉子加工活跃途径的一部分。

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