Abstract

BackgroundVibrio cholerae, a Gram-negative bacterium, is highly motile owing to the presence of a single polar flagellum. The global anaerobiosis response regulator, ArcA regulates the expression of virulence factors and enhance biofilm formation in V. cholerae. However, the function of ArcA for the motility of V. cholerae is yet to be elucidated. CytR, which represses nucleoside uptake and catabolism, is known to play a chief role in V. cholerae pathogenesis and flagellar synthesis but the mechanism that CytR influences motility is unclear.ResultsIn this study, we found that the ΔarcA mutant strain exhibited higher motility than the WT strain due to ArcA directly repressed flrA expression. We further discovered that CytR directly enhanced fliK expression, which explained why the ΔcytR mutant strain was retarded in motility. On the other hand, cytR was a direct ArcA target and cytR expression was directly repressed by ArcA. As expected, cytR expression was down-regulated.ConclusionsOverall, ArcA plays a critical role in V. cholerae motility by regulating flrA expression directly and fliK indirectly in the manner of cytR.

Highlights

  • Vibrio cholerae, a Gram-negative bacterium, is highly motile owing to the presence of a single polar flagellum

  • To evaluate the role of Anoxic redox control cognate response regulator (ArcA) in V. cholerae motility, we investigated the surface motility of : ParcA (ΔarcA) mutant strain on soft agar plates in aerobic conditions

  • ArcA directly repressed cytR expression In addition to ArcA and Cytidine repressor (CytR) being related to the V. cholerae motility, we found that CytR is a new downstream regulatory gene of ArcA

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Summary

Introduction

A Gram-negative bacterium, is highly motile owing to the presence of a single polar flagellum. The global anaerobiosis response regulator, ArcA regulates the expression of virulence factors and enhance biofilm formation in V. cholerae. The flagellum of V. cholerae is a complex self-assembling organelle that is attached to the cell surface and allows bacterial cells to move in their environment [2]; it plays a pivotal role in substrates adhesion, biofilm formation, and virulence [3,4,5,6]. Elucidating the mechanisms underlying the regulation of flagellum should enhance our understanding of the lifecycle of V. cholerae both in the intestinal and aquatic phases. V. cholerae flagellar genes are expressed within a fourtiered transcriptional hierarchy [4]. Phosphorylated ArcA is subsequently activated as a transcription factor, resulting in the up-or downregulation of several downstream genes [9, 10].

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