Open AccessGenetic dissection of Helicobacter pylori AddAB role in homologous recombination
Author(s) -
Marsin Stéphanie,
Lopes Anne,
Mathieu Aurélie,
Dizet Eléa,
Orillard Emilie,
Guérois Raphaël,
Radicella J. Pablo
Publication year - 2010
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2010.02077.x
Subject(s) - homologous recombination , biology , helicobacter pylori , recbcd , genetics , escherichia coli , mutant , dna repair , bacillus subtilis , population , phenotype , microbiology and biotechnology , dna , gene , bacteria , demography , sociology
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 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.