“In the model organism E. coli, recombination mediated by therelated XerC and XerD recombinases complexed with the FtsKtranslocase at specialized dif sites, resolves dimeric chromosomesinto free monomers to allow efficient chromosome segregation atcell division. Computational genome analysis of Helicobacterpylori, a slow growing gastric pathogen, identified just onechromosomal xer gene (xerH) and its cognate dif site (difH). Herewe show that recombination between directly repeated difH sitesrequires XerH, FtsK but not XerT, the TnPZ transposon associatedrecombinase. xerH inactivation was not lethal, but resulted inincreased DNA per cell, suggesting defective chromosomesegregation. The xerH mutant also failed to colonize mice, and wasmore susceptible to UV and ciprofloxacin, which induce DNAbreakage, and thereby recombination and chromosome dimer formation.xerH inactivation and overexpression each led to a DNA segregationdefect, suggesting a role for Xer recombination in regulation ofreplication. In addition to chromosome dimer resolution and basedon the absence of genes for topoisomerase IV (parC, parE) in H.pylori, we speculate that XerH may contribute to chromosomedecatenation, although possible involvement of H. pylori's DNAgyrase and topoisomerase III homologue are also considered. Furtheranalyses of this system should contribute to general understandingof and possibly therapy development for H. pylori, which causespeptic ulcers and gastric cancer; for the closely related,diarrheagenic Campylobacter species; and for unrelated slow growingpathogens that lack topoisomerase IV, such as Mycobacteriumtuberculosis.”

article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC332523

What is one intrinsic problem with circular DNA molecules duringhomologous recombination? How does this effect cell division?

Bacteria with circular chromosomes typically containsite-specific tyrosine Xer recombinases and dif sites. Why arethese recombinases and dif sites important to the bacterialcell?

Briefly explain how the XerC and XerD recombinases function inE.coli.

How does the H.pylori Xer recombinase system differ from theE.coli system? How is it similar?

E.coli typically removes topological links between concatenatedDNA by using topoisomerase IV. H. pylori seems to lacktopoisomerase IV. If this is the case, how does H. pylori deal withcircular DNA dimers and/or multimers?