Department of Biochemistry, University of Oxford, Oxford, UK.
Nucleic Acids Res. 2010 Jan;38(1):72-81. doi: 10.1093/nar/gkp843. Epub 2009 Oct 23.
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 FtsKgamma regulatory subdomain, which interacts with XerD, and is not dependent on either recombinase-mediated DNA cleavage activity, or the formation of synaptic complexes.
大肠杆菌 FtsK 是一种强大、快速的双链 DNA 转位酶，能够从 DNA 上剥离蛋白质。FtsK 在染色体分离的晚期通过促进姐妹染色体在分裂隔膜处解连来发挥作用。KOPS 指导的 DNA 转位将 FtsK 引导至 dif，位于复制末端区域内，ter，FtsK 在那里激活 XerCD 位点特异性重组。在这里，我们表明 FtsK 转位特异性地在 XerCD-dif 处停止，从而防止 XerCD 从 dif 中去除，并允许通过重组激活染色体解连。在 XerCD-dif 处的转位停止伴随着 FtsK ATP 酶活性的降低，并且与 FtsK 从 DNA 上的解离无关。在重组酶-DNA 复合物处的特异性停止不需要与 XerD 相互作用的 FtsKgamma 调节亚基，并且不依赖于重组酶介导的 DNA 切割活性，或形成突触复合物。
