FtsK-dependent and -independent pathways of Xer site-specific recombination
FtsK-dependent and -independent pathways of Xer site-specific recombination
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DOI：
10.1093/emboj/18.20.5724
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发表时间：
1999-10-15
期刊：
影响因子：
11.4
通讯作者：
Sherratt, DJ
中科院分区：
文献类型：
--
作者：
Recchia, GD;Aroyo, M;Sherratt, DJ
环状染色体之间的同源重组产生在细胞分裂时不能分离的二聚体。埃希氏菌coli Xer位点特异性重组将染色体和质粒二聚体转化为单体。两种重组酶XerC和XerD作用于E.大肠杆菌染色体重组位点，dif和质粒中的相关位点。我们表明，Xer重组质粒dif网站有效地发生只有当FtsK存在，并在允许染色体二聚体形成的条件下，而重组质粒网站CER和psi是独立的这些因素。我们建议，染色体二聚体和FtsK依赖的过程，激活Xer重组质粒dif也激活Xer重组染色体dif。FtsK C-末端突变导致的染色体分离缺陷可归因于Xer重组未能解析染色体二聚体。到单体。导致FtsK独立Xer重组的条件支持FtsK作用于霍利迪连接Xer重组介导的假设。
Homologous recombination between circular chromosomes generates dimers that cannot be segregated at: cell division. Escherichia. coli Xer site-specific recombination converts chromosomal and plasmid dimers to monomers. Two recombinases, XerC and XerD, act at the E. coli chromosomal recombination site, dif, and at related sites in plasmids. We demonstrate that Xer recombination at plasmid dif sites occurs efficiently only when FtsK is present and under conditions that allow chromosomal dimer formation, whereas recombination at the plasmid sites cer and psi is independent of these factors. We propose that the chromosome dimer- and FtsK-dependent process that: activates Xer recombination at plasmid dif also activates Xer recombination at chromosomal dif. The defects in chromosome segregation that result from mutation of the FtsK C-terminus are attributable to the failure of Xer recombination to resolve chromosome dimers. to monomers. Conditions that lead to FtsK-independent Xer recombination support the hypothesis that FtsK acts on Holliday junction Xer recombination inter; mediates.