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Mass, S.

Publications and source records attributed to Mass, S..

4 recordsLinked to original sources

Vibrio campbellii encodes a distinct set of type III secretion system effectors that mediate cytotoxicity in eukaryotic host models

Type III secretion systems (T3SS) are common virulence factors that facilitate the injection of anti-eukaryotic effector toxins that damage and kill target host cells. The sequence and function of the structural and regulatory proteins of these systems are conserved across Gram-negative pathogens, including Pseudomonas, Yersinia, and Salmonella. However, the identity and function of effector proteins are not conserved and are unknown in several relevant human and animal pathogens. Here, we used comparative genomics to identify and characterize the effectors encoded by Vibrio campbellii BB120, a crustacean and fish pathogen. We showed that most sequenced Vibrio strains belonging to the Harveyi clade, including V. campbellii, encode a full set of structural and regulatory genes corresponding to the T3SS1 of V. parahaemolyticus; the exception is V. natriegens. Transcriptomic and proteomic analyses identified four V. campbellii effectors that are secreted by the T3SS. Among these, two effectors are encoded outside the T3SS island, and all effector genes were co-regulated by both the master T3SS regulator ExsA and by the master quorum sensing regulator LuxR. Three effectors - VopS, CopA, and VIBHAR_06684 - exhibited toxic activity in yeast cells or bone marrow-derived macrophages, and the toxicity phenotypes were dependent on a functional T3SS. VopS and CopA are conserved among the queried species of the Harveyi clade. VIBHAR_06684 or VIBHAR_05674 did not show conservation among the queried species. These findings demonstrate that T3SSs in bacteria from the same clade have conserved structural secretion apparatuses but exhibit variance in effector repertoires. We postulate that the functions of effectors differ between species to impart roles in host specificity. Author SummaryPathogenic Vibrio bacteria employ many virulence factors to cause disease in marine animals, including biofilms, proteases, and the secretion of toxins. Here, we identify four secreted toxins encoded by V. campbellii that are toxic to eukaryotic cells. These toxins are secreted by the type III secretion system, a needle-like apparatus used by many bacteria to inject toxins into host cells. The toxins identified in this study are regulated by quorum sensing, a method bacteria use to communicate and control virulence genes required for pathogenesis. The results of this study indicate that different Vibrio species employ distinct sets of toxins that possibly facilitate their interaction with a host.

microbiology↗

Quorum Sensing Regulates Virulence Factors in the Coral Pathogen Vibrio coralliilyticus

The bacterial pathogen Vibrio coralliilyticus (Vcor) causes disease in coral species worldwide. The mechanisms of Vcor coral colonization, coral microbiome interactions, and virulence factor production are understudied. In other model Vibrio species, virulence factors like biofilm formation, toxin secretion, and protease production are controlled through a density-dependent communication system called quorum sensing (QS). 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 identify an active QS signaling pathway in two V. coralliilyticus strains with distinct infection etiologies: type strain BAA-450 and coral isolate OCN008. The inter-species AI-2 autoinducer signaling pathway in both strains controls expression of the master QS transcription factor VcpR to regulate >300 genes, including protease production, biofilm formation, and two conserved type VI secretion systems (T6SSs). Activation of T6SS1 by QS results in secretion of effectors and enables interbacterial competition and killing of prey bacteria. We conclude that the QS system in V. coralliilyticus is functional and controls expression of genes involved in relevant bacterial behaviors that may influence coral infection. IMPORTANCEVibrio coralliilyticus infects many marine organisms, including multiple species of corals, and is a primary causative agent of tissue loss diseases and bacterial-induced bleaching. Here we investigate a common cell-cell communication mechanism called quorum sensing, which is known to be intimately connected to virulence in other Vibrio species. Our genetic and chemical studies of V. coralliilyticus quorum sensing uncovered an active pathway that directly regulates key virulence factors: proteases, biofilms, and secretion systems. These findings connect bacterial signaling in communities to infection of corals, which may lead to novel treatments and earlier diagnoses of coral diseases in reefs.

microbiology↗

Bile acids activate the antibacterial T6SS1 in the gut pathogen Vibrio parahaemolyticus

The marine bacterium Vibrio parahaemolyticus is a major cause of seafood-borne gastroenteritis in humans and of acute hepatopancreatic necrosis disease in shrimp. Bile acids, produced by the host and modified into secondary bile acids by commensal bacteria in the gastrointestinal tract, induce the virulence factors leading to disease in humans and shrimp. Here, we show that secondary bile acids also activate this pathogens type VI secretion system 1 (T6SS1), a toxin-delivery apparatus mediating interbacterial competition. This finding implies that Vibrio parahaemolyticus exploits secondary bile acids to activate its virulence factors and identify the presence of commensal bacteria that it needs to outcompete in order to colonize the host. ImportanceBacterial pathogens often manipulate their host and cause disease by secreting toxic proteins. However, to successfully colonize a host, they must also remove commensal bacteria that reside in it and may compete with them over resources. Here, we find that the same host-derived molecules that activate the secreted virulence toxins in a gut bacterial pathogen, Vibrio parahaemolyticus, also activate an antibacterial toxin delivery system that targets such commensal bacteria. These findings suggest that a pathogen can use one cue to launch a coordinated, trans-kingdom attack that enables it to colonize a host.

microbiology↗

A T6SS in the coral pathogen Vibrio coralliilyticus secretes an arsenal of anti-eukaryotic effectors and contributes to virulence

Vibrio coralliilyticus (Vcor) is a pathogen of coral and shellfish, leading to devastating economic and ecological consequences worldwide. Although rising ocean temperatures correlate with increased Vcor pathogenicity, the specific molecular mechanisms and determinants contributing to virulence remain poorly understood. Here, we systematically analyzed the type VI secretion system (T6SS), a contact-dependent toxin delivery apparatus, in Vcor. We identified two omnipresent T6SSs that are activated at temperatures in which Vcor becomes virulent; T6SS1 is an antibacterial system mediating interbacterial competition, whereas T6SS2 mediates anti-eukaryotic toxicity and contributes to mortality during infection of an aquatic model organism, Artemia salina. Using comparative proteomics, we identified the T6SS1 and T6SS2 toxin arsenals of three Vcor strains with distinct disease etiologies. Remarkably, T6SS2 secretes at least nine novel anti-eukaryotic toxins comprising core and accessory repertoires. We propose that T6SSs differently contribute to Vcors virulence: T6SS2 plays a direct role by targeting the host, while T6SS1 plays an indirect role by eliminating competitors. Author SummaryCoral reefs are diverse ecosystems providing habitats for various fish, invertebrates, and microorganisms. Climate change, leading to rising ocean water temperatures, correlates with coral bleaching and mass mortality events. An implicated causal agent of coral disease outbreaks is the marine bacterium Vibrio coralliilyticus. Here, we found that two toxin injection systems present in all Vibrio coralliilyticus strains are regulated by temperature; we revealed the toxins that they secrete and their function in competition against rival bacteria and in the intoxication of an animal host. Our findings implicate these systems as previously unappreciated contributors to Vibrio coralliilyticus virulence, illuminating possible targets to treat or prevent coral infection.

microbiology↗