Participation of CheR and CheB in the chemosensory response of Campylobacter jejuni

Campylobacter jejuni is a leading cause of bacterial gastroenteritis in humans and a commensal bacterium of the intestinal tracts of animals, especially poultry. Chemotaxis is an important determinant for chicken colonization of C. jejuni. Adaptation has a crucial role in the gradient-sensing mechanism that underlies chemotaxis. The genome sequence of C. jejuni reveals the presence of genes encoding putative adaptation proteins, CheB and CheR. In-frame deletions of cheB, cheR and cheBR were constructed and the chemosensory behaviour of the resultant mutants was examined on swarm plates. CheB and CheR proteins significantly influence chemotaxis but are not essential for this behaviour to occur. Increased mobility of two methyl-accepting chemotaxis proteins (MCPs), DocC and Tip1, during SDS-PAGE was detected in the mutants lacking functional CheB in the presence of CheR, presumably resulting from stable methylation of receptors. In vitro studies using tissue culture revealed that deletion of cheR resulted in hyperadherent and hyperinvasive phenotypes, while deletion of cheB resulted in nonadherent, noninvasive phenotypes. Furthermore, the Delta cheBR mutant showed significantly reduced ability to colonize chick caeca. Our data suggest that modification of chemoreceptors by the CheBR system is involved in regulation of chemotaxis in C. jejuni although CheB is apparently not controlled by phosphorylation.