Abstract
In many bacteria, including Vibrio cholerae, cyclic dimeric guanosine monophosphate (c-di-GMP) controls the motile to biofilm life style switch. Yet, little is known about how this occurs. In this study, we report that changes in c-di-GMP concentration impact the biosynthesis of the MshA pili, resulting in altered motility and biofilm phenotypes in V. cholerae. Previously, we reported that cdgJ encodes a c-di-GMP phosphodiesterase and a ΔcdgJ mutant has reduced motility and enhanced biofilm formation. Here we show that loss of the genes required for the mannose-sensitive hemagglutinin (MshA) pilus biogenesis restores motility in the ΔcdgJ mutant. Mutations of the predicted ATPase proteins mshE or pilT, responsible for polymerizing and depolymerizing MshA pili, impair near surface motility behavior and initial surface attachment dynamics. A ΔcdgJ mutant has enhanced surface attachment, while the ΔcdgJmshA mutant phenocopies the high motility and low attachment phenotypes observed in a ΔmshA strain. Elevated concentrations of c-di-GMP enhance surface MshA pilus production. MshE, but not PilT binds c-di-GMP directly, establishing a mechanism for c-di-GMP signaling input in MshA pilus production. Collectively, our results suggest that the dynamic nature of the MshA pilus established by the assembly and disassembly of pilin subunits is essential for transition from the motile to sessile lifestyle and that c-di-GMP affects MshA pilus assembly and function through direct interactions with the MshE ATPase.
Highlights
Vibrio cholerae, the causative agent of the human intestinal disease cholera, is a natural inhabitant of aquatic ecosystems [1]
We demonstrate that c-di-GMP promotes the production of a cell surface structure called mannose-sensitive hemagglutinin (MshA) pili by binding the molecular motor responsible for polymerizing pilus subunits
This study identifies a novel mechanism for c-di-GMP regulation of pilus production through interactions with the molecular motor responsible for pilus assembly
Summary
The causative agent of the human intestinal disease cholera, is a natural inhabitant of aquatic ecosystems [1]. The bacteria turn on regulatory networks that facilitate bacterial growth and survival during the infection process [2]. They activate production of virulence factors including the toxin-coregulated pilus (TCP), essential for intestinal colonization, and the cholera toxin (CT), responsible for production of massive watery diarrhea that results in dissemination of V. cholerae back to aquatic ecosystems [3]. Growth in a biofilm induces a hyper-infectious phenotype [9]. These studies highlight the importance of the biofilm growth mode in both the intestinal and aquatic phases of the V. cholerae life cycle
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