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Crisan, C. V.

Publications and source records attributed to Crisan, C. V..

2 recordsLinked to original sources

Accumulation of dead cells from contact killing facilitates coexistence in bacterial biofilms

Bacterial communities govern their composition using a wide variety of social interactions, some of which are antagonistic. Many antagonistic mechanisms, such as the Type VI Secretion System (T6SS), require killer cells to directly contact target cells. The T6SS is hypothesized to be a highly potent weapon, capable of facilitating the invasion and defense of bacterial populations. However, we find that the efficacy of the T6SS is severely limited by the material consequences of cell death. Through experiments with Vibrio cholerae strains that kill via the T6SS, we show that dead cell debris quickly accumulates at the interface that forms between competing strains, preventing contact and thus preventing killing. While previous experiments have shown that T6SS killing can reduce a population of target cells by as much as one-million-fold, we find that as a result of the formation of dead cell debris barriers, the impact of T6SS killing depends sensitively on the initial concentrations of killer and target cells. Therefore, while the T6SS provides defense against contacting competitors on a single cell level, it is incapable of facilitating invasion or the elimination of competitors on a community level.

microbiology↗

Analysis of Vibrio cholerae genomes using a novel bioinformatic tool identifies new, active Type VI Secretion System gene clusters

BackgroundLike many bacteria, Vibrio cholerae, which causes fatal cholera, deploys a harpoon-like Type VI Secretion System (T6SS) to compete against other microbes in environmental and host settings. The T6SS punctures adjacent cells and delivers toxic effector proteins that are harmless to bacteria carrying cognate immunity factors. Only four effector/immunity pairs encoded on one large and three auxiliary gene clusters have been characterized from largely clonal, patient-derived strains of V. cholerae. ResultsWe sequenced two dozen V. cholerae strain genomes from diverse sources and developed a novel and adaptable bioinformatic tool based on Hidden Markov Models. We identified two new T6SS auxiliary gene clusters; one, Aux 5, is described here. Four Aux 5 loci are present in the host strain, each with an atypical effector/immunity gene organization. Structural prediction of the putative effector indicated it is a lipase, which we name TleV1 (Type VI lipase effector Vibrio, TleV1). Ectopic TleV1 expression induced toxicity in E. coli, which was rescued by co-expression of the TleV1 immunity factor. A clinical V. cholerae reference strain expressing the Aux 5 cluster used TleV1 to lyse its parental strain upon contact via its T6SS but was unable to kill parental cells expressing TleV1s immunity factor. ConclusionWe developed a novel bioinformatic method and identified new T6SS gene clusters in V. cholerae. We also showed the TleV1 toxin is delivered in a T6SS-manner by V. cholerae and can lyse other bacterial cells. Our web-based tool may be modified to identify additional novel T6SS genomic loci in diverse bacterial species.

microbiology↗