Interestingly, several slow growing bacterial pathogenic genera, including Helicobacter, Campylobacter and Mycobacterium, lack parC and parE topoisomerase IV subunit genes . Further complicating inferences about XerH action in the case of H. pylori, many strains contain a second divergent xer recombinase gene, xerT, generally within a large TnPZ transposon . Although its encoded XerT protein is needed for transposon excision and conjugative transfer, and probably also functions as a transposase, the possibility of XerT collaborating with XerH for chromosome resolution also merited testing. The experiments presented here demonstrate site-specific recombination at H. pylori difH sites, and show that it requires XerH, FtsK and an intact difH sequence, but not XerT, and bring into focus the need to learn how catenanes are processed in the many other slow growing human pathogens that, like H. pylori, lack topoisomerase IV. Under our conditions, no streptomycin resistant colonies were obtained when the 40 bp yeast DNA sequence flanked the rpsL-cat cassette. In contrast, many streptomycin resistant colonies were obtained in strains in which difH flanked rpsL-cat. All of these streptomycin resistant colonies were chloramphenicol sensitive. PCR confirmed that streptomycin sensitive clones still contained the full-length difH repeat cassette and that rpsL-cat was absent from streptomycin resistant clones. As expected, DNA sequencing confirmed that a single difH ����scar���� sequence had been retained in these streptomycin resistant, chloramphenicol sensitive excisants, . The frequency of XerH recombination at difH sites at the ureAB locus was also evaluated using this difH repeat cassette. Cells were grown for 2 and 4 days in non-selective GSI-IX Gamma-secretase inhibitor medium , streaked out for single colony AZD2281 isolates, and 100�C200 colonies were then tested for streptomycin/chloramphenicol resistance/susceptibility phenotypes. Figure 1C shows that the difH recombination frequency is significantly higher for the cassette placed at ureAB than at HP0203-HP0204 after 4 days culture. We conclude that the chromosomal position of paired difH sites affects the frequency of recombination between them. Erythroid CR1 is a ligand used by P. falciparum merozoites for sialic acid-independent invasion of red blood cells . Moreover, CR1 on non-parasitized erythrocytes is a ligand for P. falciparum erythrocyte membrane protein 1 borne on infected erythrocytes; this interaction mediates formation of ����rosettes����, which consist of clusters of infected and non-infected cells . Rosette formation is associated with life-threatening forms of cerebral malaria .