The Campylobacter jejuni response regulator and cyclic-Di-GMP binding CbrR is a novel regulator of flagellar motility

Claudia A. Cox, Marek Bogacz, Faiha M. El Abbar, Darren D. Browning, Brian Y. Hsueh, Chris M. Waters, Vincent T. Lee, Stuart A. Thompson

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


A leading cause of bacterial gastroenteritis, Campylobacter jejuni is also associated with broad sequelae, including extragastrointestinal conditions such as reactive arthritis and Guillain-Barré Syndrome (GBS). CbrR is a C. jejuni response regulator that is annotated as a diguanylate cyclase (DGC), an enzyme that catalyzes the synthesis of c-di-GMP, a universal bacterial second messenger, from GTP. In C. jejuni DRH212, we constructed an unmarked deletion mutant, cbrR, and complemented mutant, cbrR+. Motility assays indicated a hyper-motile phenotype associated with cbrR, whereas motility was deficient in cbrR+. The overexpression of CbrR in cbrR+ was accompanied by a reduction in expression of FlaA, the major flagellin. Biofilm assays and scanning electron microscopy demonstrated similarities between DRH212 and cbrR; however, cbrR+ was unable to form significant biofilms. Transmission electron microscopy showed similar cell morphology between the three strains; however, cbrR+ cells lacked flagella. Differential radial capillary action of ligand assays (DRaCALA) showed that CbrR binds GTP and c-di-GMP. Liquid chromatography tandem mass spectrometry detected low levels of c-di-GMP in C. jejuni and in E. coli expressing CbrR. CbrR is therefore a negative regulator of FlaA expression and motility, a critical virulence factor in C. jejuni pathogenesis.

Original languageEnglish (US)
Article number86
Issue number1
StatePublished - Jan 2022


  • Biofilm
  • C-di-GMP
  • Flagella
  • Motility
  • Pathogenesis
  • Regulation

ASJC Scopus subject areas

  • Microbiology
  • Microbiology (medical)
  • Virology


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