The nucleotide excision repair (NER) system of Helicobacter pylori: role in mutation prevention and chromosomal import patterns after natural transformation.

Background: Extensive genetic diversity and rapid allelic diversification are characteristics of the human gastric pathogen Helicobacter pylori, and are believed to contribute to its ability to cause chronic infections. Both a high mutation rate and frequent imports of short fragments of exogenous DNA during mixed infections play important roles in generating this allelic diversity. In this study, we used a genetic approach to investigate the roles of nucleotide excision repair (NER) pathway components in H.

Mosaic DNA imports with interspersions of recipient sequence after natural transformation of Helicobacter pylori.

Helicobacter pylori colonizes the gastric mucosa of half of the human population, causing gastritis, ulcers, and cancer. H. pylori is naturally competent for transformation by exogenous DNA, and recombination during mixed infections of one stomach with multiple H.

The Helicobacter pylori mutY homologue HP0142 is an antimutator gene that prevents specific C to A transversions.

Extensive genetic variability resulting from a high mutation rate and frequent recombination is a characteristic of Helicobacter pylori. Its average mutation rate is 1 x 10(-6), similar to that of Escherichia coli mutator strains. Few genes involved in DNA repair have been functionally characterized in H.