Dataset Information

Vibrio cholerae represses polysaccharide synthesis to promote motility in mucosa.

ABSTRACT: The viscoelastic mucus layer of gastrointestinal tracts is a host defense barrier that a successful enteric pathogen, such as Vibrio cholerae, must circumvent. V. cholerae, the causative agent of cholera, is able to penetrate the mucosa and colonize the epithelial surface of the small intestine. In this study, we found that mucin, the major component of mucus, promoted V. cholerae movement on semisolid medium and in liquid medium. A genome-wide screen revealed that Vibrio polysaccharide (VPS) production was inversely correlated with mucin-enhanced motility. Mucin adhesion assays indicated that VPS bound to mucin. Moreover, we found that vps expression was reduced upon exposure to mucin. In an infant mouse colonization model, mutants that overexpressed VPS colonized less effectively than wild-type strains in more distal intestinal regions. These results suggest that V. cholerae is able to sense mucosal signals and modulate vps expression accordingly so as to promote fast motion in mucus, thus allowing for rapid spread throughout the intestines.

SUBMITTER: Liu Z

PROVIDER: S-EPMC4333447 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature

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Vibrio cholerae represses polysaccharide synthesis to promote motility in mucosa.

Liu Zhenyu Z Wang Yuning Y Liu Shengyan S Sheng Ying Y Rueggeberg Karl-Gustav KG Wang Hui H Li Jie J Gu Frank X FX Zhong Zengtao Z Kan Biao B Zhu Jun J

Infection and immunity 20150105 3

The viscoelastic mucus layer of gastrointestinal tracts is a host defense barrier that a successful enteric pathogen, such as Vibrio cholerae, must circumvent. V. cholerae, the causative agent of cholera, is able to penetrate the mucosa and colonize the epithelial surface of the small intestine. In this study, we found that mucin, the major component of mucus, promoted V. cholerae movement on semisolid medium and in liquid medium. A genome-wide screen revealed that Vibrio polysaccharide (VPS) pr ...[more]

PMID: 25561707

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Project description:Motility is required for many bacterial pathogens to reach and colonize target sites. Vibrio cholerae traverses a thick mucus barrier coating the small intestine to reach the underlying epithelium. We screened a transposon library in motility medium containing mucin to identify factors that influence mucus transit. Lesions in structural genes of the type VI secretion system (T6SS) were among those recovered. Two-dimensional (2D) and 3D single-cell tracking was used to compare the motility behaviors of wild-type cells and a mutant that collectively lacked three essential T6SS structural genes (T6SS-). In the absence of mucin, wild-type and T6SS- cells exhibited similar speeds and run-reverse-flick (RRF) swimming patterns, in which forward-moving cells briefly backtrack before stochastically reorienting (flicking) in a new direction upon resuming forward movement. We show that mucin induced T6SS expression and activity in wild-type bacteria but significantly decreased their swimming speed and flicking, yielding curvilinear or near-surface circular traces for many cells. Conversely, mucin slowed T6SS- cells to a lesser extent, and many continued to flick and produce RRF-like traces. ΔcheY3 cells, which exclusively swim in the forward direction and thus cannot flick, also produced curvilinear traces with or without mucin present and, on occasion, near-surface circular traces in the presence of mucin. The dependence of flicking on swimming speed suggested that mucin-induced T6SS activity further decreased V. cholerae motility and thereby reduced flicking probability during reverse-to-forward transitions. We propose that this encourages cells to continue on their current trajectory rather than reorienting, which may benefit those tracking toward the epithelial surface.IMPORTANCEV. cholerae deploys an arsenal of virulence factors as it attempts to traverse a protective mucus layer and reach the epithelial surface of the distal small intestine. The T6SS used to cull bacterial competition during infection is induced by mucus. We show that this activity may serve an additional purpose by further decreasing motility in the presence of mucin, thereby reducing the probability of speed-dependent, near-perpendicular directional changes. We posit that this encourages cells to maintain course rather than change direction, which may aid those attempting to reach and colonize the epithelial surface.

Dataset Information

Vibrio cholerae represses polysaccharide synthesis to promote motility in mucosa.

Publications

Vibrio cholerae represses polysaccharide synthesis to promote motility in mucosa.

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