Project description:The bacterial pathogen Vibrio coralliilyticus infects a variety of marine organisms globally and causes early onset of disease in multiple coral species. The etiology of coral disease and relative pathogenicity of V. coralliilyticus strains is well-documented, but the mechanisms of V. coralliilyticus coral colonization, virulence factor production, and interactions with coral microbiome are understudied. Many virulence factors responsible for pathogenic behaviors are controlled through a density-dependent, bacterial communication system called quorum sensing (QS). In other Vibrio species, behaviors like bioluminescence, biofilm formation, toxin secretion, and protease production are controlled via the master quorum sensing transcriptional regulator called LuxR/HapR. Comparative genomics indicated that V. coralliilyticus genomes share high sequence identity for most of the QS signaling and regulatory components identified in other Vibrio species. Here, we characterize active components of the V. coralliilyticus QS system and identify the VcpR (LuxR/HapR homolog) regulons in two strains with distinct infection etiologies. We show that VcpR transcription is dependent on signaling by autoinducer AI-2, whereas we were unable to detect production of acyl-homoserine lactone autoinducers. The VcpR regulator controls expression of >200 genes in both the type strain BAA-450 and isolate OCN008, including two genes encoding proteases (VcpA and VcpB) known to impact coral infection. In both isolates, VcpR activates the expression of Type VI Secretion System genes from both systems 1 and 2, which results in interbacterial competition and killing of prey bacteria. We conclude that the QS system in V. coralliilyticus is active and controls expression of genes involved in relevant bacterial behaviors that may influence coral infection.
Project description:Comparative proteomics to identify the proteins secreted by T6SS1 and T6SS2 of Vibrio coralliilyticus strains BAA-450, OCN008, and OCN014.
