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“Helicobacter pylori infects the stomach of about half of the world’s human population, frequently causing chronic inflammation at the origin of several gastric pathologies. One of the most remarkable characteristics of the species is its remarkable genomic plasticity in which homologous recombination (HR) plays

a critical role. Here, we analyzed the role of the H. pylori homologue of the AddAB recombination protein. Bioinformatics analysis of the proteins unveils the similarities and differences of the H. pylori AddAB complex with respect to the Selleckchem Atezolizumab RecBCD and AddAB complexes from Escherichia coli and Bacillus subtilis, respectively. Helicobacter pylori mutants lacking functional addB or/and addA show the same level of sensitivity to DNA-damaging agents such as UV or irradiation and of deficiency in intrachromosomal RecA-dependent HR. Epistasis analyses of both DNA repair and HR phenotypes, using double and triple

recombination mutants, demonstrate that, in H. pylori, AddAB and RecOR complexes define two separate presynaptic pathways with little functional overlap. However, neither of these complexes participates in the RecA-dependent process of transformation of these naturally competent bacteria. The pathogen Helicobacter pylori colonizes the stomach mucosa of about half of the human population, frequently resulting in chronic gastritis, which can lead to peptic ulcers

and, in a small fraction of cases, to cancer. Adaptation of H. pylori to the changing gastric environment within BTK inhibitors library a host, or to new hosts, suggests an enhanced ability of this pathogen to change. Indeed, H. pylori is one of the most genetically diverse bacterial species. At the origin of such diversity are both mutations and recombination events (Suerbaum & Josenhans, 2007). Incorporation of DNA sequences by homologous recombination (HR) into the H. pylori chromosome, facilitated by the natural competence of this species, is crucial for horizontal gene transfer between unrelated strains colonizing the same host (Kersulyte et al., 1999). This process is believed to be the cause of its panmictic population structure (Suerbaum et al., 1998). Analysis of the genomic sequences has also underlined the importance of intragenomic Org 27569 chromosomal rearrangements mediated by HR (Israel et al., 2001; Aras et al., 2003). In Escherichia coli, two major DNA recombination initiation (presynaptic) pathways coexist and are complementary: the RecFOR and the RecBCD pathways. The RecFOR pathway is essential for the postreplication repair of gaps and for the restart of replication following UV damage. However, none of the recF, recO and recR mutants show a decrease in HR following conjugation or transduction (Howard-Flanders & Bardwell, 1981; Kuzminov, 1999; Ivancic-Bace et al., 2003). We recently reported the presence in H.