Small non-coding RNA CjNC110 influences motility, autoagglutination, AI-2 localization, hydrogen peroxide sensitivity and chicken colonization in Campylobacter jejuni
A. J. Kreuder, B. Ruddell, K. Mou, A. Hassall, Q. Zhang, P. J. Plummer
Abstract
Small non-coding RNAs are involved in many important physiological functions in pathogenic microorganisms. Previous studies have identified the presence of non-coding RNAs in the major zoonotic pathogen Campylobacter jejuni, however, few have been functionally characterized to date. CjNC110 is a conserved ncRNA in C. jejuni, located downstream of the luxS gene which is responsible for the production of the quorum-sensing molecule autoinducer-2 (AI-2). In this study, we utilized strand specific high-throughput RNAseq to identify potential targets or interactive partners of CjNC110 in a sheep abortion clone of C. jejuni. This data was then utilized to focus further phenotypic evaluation of the role of CjNC110 in motility, autoagglutination, quorum sensing, hydrogen peroxide sensitivity and chicken colonization in C. jejuni. Inactivation of the CjNC110 ncRNA led to a statistically significant decrease in autoagglutination ability as well as increased motility and hydrogen peroxide sensitivity when compared to wild-type. Extracellular AI-2 detection was decreased in {Delta}CjNC110, however, intracellular AI-2 accumulation was significantly increased, suggesting a key role of CjNC110 in modulating the transport of AI-2. Notably, {Delta}CjNC110 also showed a decreased ability to colonize chickens. Complementation of CjNC110 restored all phenotypic changes back to wild-type levels. The collective results of the phenotypic and transcriptomic changes observed in our data provide valuable insights into the pathobiology of C. jejuni sheep abortion clone and strongly suggest that CjNC110 plays an important role in regulation of energy taxis, flagellar glycosylation, cellular communication via quorum sensing, oxidative stress tolerance and chicken colonization in this important zoonotic pathogen.
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