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FtsK translocation on DNA stops at XerCD-dif.

机译:DNA上的FtsK易位在XerCD-dif处停止。

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Escherichia coli FtsK is a powerful, fast, double-stranded DNA translocase, which can strip proteins from DNA. FtsK acts in the late stages of chromosome segregation by facilitating sister chromosome unlinking at the division septum. KOPS-guided DNA translocation directs FtsK towards dif, located within the replication terminus region, ter, where FtsK activates XerCD site-specific recombination. Here we show that FtsK translocation stops specifically at XerCD-dif, thereby preventing removal of XerCD from dif and allowing activation of chromosome unlinking by recombination. Stoppage of translocation at XerCD-dif is accompanied by a reduction in FtsK ATPase and is not associated with FtsK dissociation from DNA. Specific stoppage at recombinase-DNA complexes does not require the FtsK gamma regulatory subdomain, which interacts with XerD, and is not dependent on either recombinase-mediated DNA cleavage activity, or the formation of synaptic complexes.
机译:大肠杆菌FtsK是一种功能强大,快速的双链DNA转移酶,可以从DNA中剥离蛋白质。 FtsK通过促进姊妹染色体在分裂间隔处的解链作用而在染色体分离的后期起作用。 KOPS指导的DNA易位将FtsK引向位于复制末端区域ter之内的dif,在该区域FtsK激活XerCD位点特异性重组。在这里,我们显示FtsK易位特别在XerCD-dif处停止,从而防止从dif去除XerCD,并允许通过重组激活染色体解链。 XerCD-dif处转位的停止伴随FtsK ATPase的减少,与FtsK从DNA的解离无关。重组酶-DNA复合物的特异性终止不需要FtsKγ调节子域,该子域与XerD相互作用,并且不依赖于重组酶介导的DNA裂解活性或突触复合物的形成。

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