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The CprS sensor kinase of the zoonotic pathogen Campylobacter jejuni influences biofilm formation and is required for optimal chick colonization
Author(s) -
Svensson Sarah L.,
Davis Lindsay M.,
MacKichan Joanna K.,
Allan Brenda J.,
Pajaniappan Mohanasundari,
Thompson Stuart A.,
Gaynor Erin C.
Publication year - 2009
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2008.06534.x
Subject(s) - biofilm , campylobacter jejuni , biology , downregulation and upregulation , microbiology and biotechnology , mutant , pathogen , motility , campylobacter , secretion , oxidative stress , colonization , virulence , bacteria , gene , biochemistry , genetics
Summary Campylobacter jejuni , a prevalent cause of bacterial gastroenteritis, must adapt to different environments to be a successful pathogen. We previously identified a C. jejuni two‐component regulatory system (Cj1226/7c) as upregulated during cell infections. Analyses described herein led us to designate the system CprRS ( C ampylobacter p lanktonic growth r egulation). While the response regulator was essential, a cprS sensor kinase mutant was viable. The Δ cprS mutant displayed an apparent growth defect and formed dramatically enhanced and accelerated biofilms independent of upregulation of previously characterized surface polysaccharides. Δ cprS also displayed a striking dose‐dependent defect for colonization of chicks and was modestly enhanced for intracellular survival in INT407 cells. Proteomics analyses identified changes consistent with modulation of essential metabolic genes, upregulation of stress tolerance proteins, and increased expression of MOMP and FlaA. Consistent with expression profiling, we observed enhanced motility and secretion in Δ cprS , and decreased osmotolerance and oxidative stress tolerance. We also found that C. jejuni biofilms contain a DNase I‐sensitive component and that biofilm formation is influenced by deoxycholate and the metabolic substrate fumarate. These results suggest that CprRS influences expression of factors important for biofilm formation, colonization and stress tolerance, and also add to our understanding of C. jejuni biofilm physiology.