Microorganisms | |
The Campylobacter jejuni Response Regulator and Cyclic-Di-GMP Binding CbrR Is a Novel Regulator of Flagellar Motility | |
Darren D. Browning1  Vincent T. Lee2  Stuart A. Thompson3  Marek Bogacz3  Claudia A. Cox3  Faiha M. El Abbar3  Brian Y. Hsueh4  Chris M. Waters4  | |
[1] Department of Biochemistry and Molecular Biology, Augusta University, Augusta, GA 30912, USA;Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, USA;Department of Medicine, Division of Infectious Diseases, Augusta University, Augusta, GA 30912, USA;Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824, USA; | |
关键词: flagella; motility; c-di-GMP; regulation; pathogenesis; biofilm; | |
DOI : 10.3390/microorganisms10010086 | |
来源: DOAJ |
【 摘 要 】
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.
【 授权许可】
Unknown