FtsK is anchored at incipient cell division septa, and interacts with a set of oriented and highly repeated 8 bp named KOPS sequences . The E. coli chromosome��s dif region is rich in KOPS sites, which are in opposite orientation on each side of the dif site. Orientationspecific KOPS recognition and asymmetry in the KOPS distribution direct FtsK-chromosome interactions to effectively guide presentation of dif to the XerC-XerD complex for recombination. FtsK interacts specifically with the XerD component of the XerCD complex and with several other proteins including Topoisomerase IV, which are likely to be LY2835219 CDK inhibitor important for efficient, well-regulated chromosome separation and segregation . Many thousands of topological links arise as circular chromosomal DNAs are unwound during replication . In E. coli interlocked chromosomes are resolved efficiently to monomers by topoisomerase IV , which is essential , primarily because of its high capacity to resolve interlocked chromosomes, and thereby allow efficient chromosome segregation, apace with rapid cell division . Of note, DNA gyrase and Xer LY2157299 TGF-beta inhibitor recombination may play secondary roles in decatenation . This is illustrated by the ability of E. coli��s XerCD-dif-FtsK system can substitute for topoisomerase IV to remove catenane links between circular DNAs in vitro without topoisomerase IV ; and the suppression of a temperature sensitive topoisomerase IV mutation by XerCD-dif recombination in E. coli producing an engineered FtsK protein with no septum anchor that is thus soluble in the cytoplasm . This Xer-mediated resolution of catenated DNAs entails multiple interconversions of catenated monomers and knotted dimers, removing a link at each step. Xer/dif recombination systems have been detected computationally in many phyla including Proteobacteria , Firmicutes and Archae . Our in silico analyses revealed that more than 85% proteobacterial species contain a conventional E. coli-type system in which related XerC and XerD recombinases act as heterodimers on cognate dif sites, with each Xer protein having a distinct role. However, Helicobacter pylori, the gastric pathogen implicated in peptic ulcer disease and gastric cancer, was inferred to contain just a single Xer recombinase, which was named XerH, as do the related Campylobacters, which cause diarrheal disease, and all other members of H. pylori��s epsilon subgroup of Gram negative proteobacteria . Single Xer recombinase systems were also found in the Gram positive Streptococci and Lactococci and in Archaea . ftsK homologues are found in nearly all eubacterial species including the epsilon proteobacteria and Streptococci and Lactococci.