Polymorphisms of the acid sensing histidine kinase gene arsS in Helicobacter pylori populations from anatomically distinct gastric sites

• Published in: Microbial pathogenesis 2012-11, Vol.53 (5-6), p.227-233
• Main Authors: Hallinger, Daniel R., Romero-Gallo, Judith, Peek, Richard M., Forsyth, Mark H.
• Format: Article
• Language: English
• Subjects: Acclimation; acid tolerance; Adaptations; Aged; Alleles; Amplified fragment length polymorphism; Amplified Fragment Length Polymorphism Analysis; arsS; Bacteriology; Biological and medical sciences; Contingency; Cytidine - genetics; Cytosine; Data processing; DNA, Bacterial - chemistry; DNA, Bacterial - genetics; Female; Fundamental and applied biological sciences. Psychology; Gastric Mucosa - microbiology; Gene expression; Gene polymorphism; Genotype; Helicobacter pylori; Helicobacter pylori - enzymology; Helicobacter pylori - genetics; Helicobacter pylori - isolation & purification; Histidine Kinase; Homopolymeric tract; Humans; Male; Microbiology; Middle Aged; Miscellaneous; Niches; patients; Phase variations; Polymorphism; Polymorphism, Genetic; Population genetics; Protein Kinases - genetics; Sequence Analysis, DNA; Sequence Deletion; Survival
• ISSN: 0882-4010; 1096-1208
• DOI: 10.1016/j.micpath.2012.08.002

Phase variation is frequently utilized by bacterial species to affect gene expression such that phenotypic variants are maintained within populations, ensuring survival as environmental or host conditions change. Unusual among Helicobacter pylori phase variable or contingency genes is arsS, encoding a sensory histidine kinase involved in the acid acclimation of the organism. The presence of a 3′ homopolymeric cytosine tract of variable length in arsS among Helicobacter pylori strains allows for the expression of various functional ArsS isoforms, differing in carboxy-terminal protein domains. In this study, we analyzed this 3′arsS region via amplified fragment length polymorphism (AFLP) and sequencing analyses for H. pylori populations from 3 different gastric sites of 12 patients. Our data indicate the presence of multiple arsS alleles within each population of H. pylori derived from the gastric antrum, cardia, or corpus of these patients. We also show that H. pylori, derived from the same anatomical site and patient, are predicted to express multiple ArsS isoforms in each population investigated. Furthermore, we identify a polymorphic deletion within arsS that generates another alternate ArsS C-terminal end. These findings suggest that four C-terminal variations of ArsS adds to the complexity of the ArsRS acid adaptation mechanism as a whole and may influence the ability of H. pylori to persist in the gastric niche for decades. ► arsS is polymorphic at its homopolymeric cytosine tract within Helicobacter pylori populations. ► H. pylori populations are predicted to express multiple variant ArsS C-terminal domains. ► A previously unrecognized ArsS C-terminal domain was documented in this study. ► Polyclonal infections of H. pylori may be common this patient group.