Abstract
Vibrio cholerae is the causative agent of cholera, a notorious diarrheal disease that is typically transmitted via contaminated drinking water. The current pandemic agent, the El Tor biotype, has undergone several genetic changes that include horizontal acquisition of two genomic islands (VSP-I and VSP-II). VSP presence strongly correlates with pandemicity; however, the contribution of these islands to V. cholerae's life cycle, particularly the 26-kb VSP-II, remains poorly understood. VSP-II-encoded genes are not expressed under standard laboratory conditions, suggesting that their induction requires an unknown signal from the host or environment. One signal that bacteria encounter under both host and environmental conditions is metal limitation. While studying V. cholerae's zinc-starvation response in vitro, we noticed that a mutant constitutively expressing zinc starvation genes (Δzur) congregates at the bottom of a culture tube when grown in a nutrient-poor medium. Using transposon mutagenesis, we found that flagellar motility, chemotaxis, and VSP-II encoded genes were required for congregation. The VSP-II genes encode an AraC-like transcriptional activator (VerA) and a methyl-accepting chemotaxis protein (AerB). Using RNA-seq and lacZ transcriptional reporters, we show that VerA is a novel Zur target and an activator of the nearby AerB chemoreceptor. AerB interfaces with the chemotaxis system to drive oxygen-dependent congregation and energy taxis. Importantly, this work suggests a functional link between VSP-II, zinc-starved environments, and energy taxis, yielding insights into the role of VSP-II in a metal-limited host or aquatic reservoir.
Highlights
The Gram-negative bacterium Vibrio cholerae, the causative agent of cholera [1], is welladapted to two distinct lifestyles: as a colonizer of macroinvertebrates in the aquatic environment and as a potentially lethal pathogen inside the human intestine [2]
We found that flagellar motility, chemotaxis, and Vibrio cholerae’s mysterious Seventh Pandemic island (VSP-II) encoded genes were required for congregation
The Vibrio Seventh Pandemic island was horizontally acquired by the El Tor pandemic strain, but its role in pathogenicity or environmental persistence is unknown
Summary
The Gram-negative bacterium Vibrio cholerae, the causative agent of cholera [1], is welladapted to two distinct lifestyles: as a colonizer of macroinvertebrates in the aquatic environment and as a potentially lethal pathogen inside the human intestine [2]. The remaining uncharacterized genes are predicted to encode transcriptional regulators (VC0497, VC0513), ribonuclease H (VC0498), a type IV pilin (VC0502), a DNA repair protein (VC0510), methyl-accepting chemotaxis proteins (VC0512, VC0514), a cyclic di-GMP phosphodiesterase (VC0515), and hypothetical proteins [23]. It is unclear if or how VSP-II enhances the pathogenicity or environmental fitness of El Tor. Intriguingly, VSP-II genes are not expressed under standard laboratory conditions [28], suggesting that their induction requires an unknown signal from the host or environment
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