Biology subjects

Santoriello, F. J.

Publications and source records attributed to Santoriello, F. J..

4 recordsLinked to original sources

bioRxiv2026

Competing Inter-Domain Quorum-Sensing Systems Control Prophage Lysis-Lysogeny Decisions

Phaeobacter inhibens T5T harbors three LuxI/LuxR quorum-sensing systems: one encoded by the host and one in each of two prophages. Each prophage quorum-sensing autoinducer activates its own lysogeny program and that of the co-resident prophage. By driving competitors toward lysogeny, prophages deny their rivals access to susceptible hosts. One prophage engages in a bidirectional interaction with the host: the prophage activates host quorum sensing, while the host represses prophage quorum sensing. Because the host and prophage autoinducers exert opposing effects on the same prophage promoter, the prophages lysis-lysogeny decision depends on the ratio of the two autoinducers rather than their absolute concentrations. Ratiometric sensing allows the prophage to infer the relative abundances of infected and uninfected hosts and to commit to lysis only when uninfected hosts predominate. Phage quorum-sensing modules are widespread and undergo diversification and exchange. These findings reveal how prophages surveil and manipulate competitors that share chemical environments.

microbiology↗

bioRxiv2025

A family of linear plasmid phages that detect a quorum-sensing autoinducer exists in multiple bacterial species

Temperate phages oscillate between lysogeny, a genomic maintenance state within a bacterial host, and lytic replication, in which the host is killed, and newly made phage particles are released. Successful transmission to new hosts requires that temperate phages appropriately time their transitions from lysogeny to lysis. It is well understood that temperate phages trigger lysis upon detection of host cell stress. Understanding of the breadth of cues that induce lysis expanded with the discovery of phages carrying quorum-sensing receptor genes that promote lytic induction exclusively at high host cell density. Bacteria engage in a cell-cell communication process called quorum sensing, which relies on the production, release, accumulation, and group-wide detection of extracellular signal molecules called autoinducers. Bacteria use quorum sensing to monitor changes in population density and synchronize collective behaviors. The temperate phage VP882 ({varphi}VP882) encodes VqmA{varphi} - a homolog of its hosts quorum-sensing receptor/transcription factor VqmA. VqmA{varphi} allows {varphi}VP882 to detect the accumulation of the host autoinducer called DPO. Presumably, launching the lytic induction program at high host cell density maximizes {varphi}VP882 transmission to new hosts. Here, by mining sequence databases for linear plasmid phages, we identify VP882-like phages in multiple DPO-producing bacterial species isolated at diverse times and geographic locations. We show that the VqmA{varphi} homologs can indeed detect DPO and, in response, activate the lytic pathway. Our observation indicates that {varphi}VP882 is a member of a large family of globally-dispersed quorum-sensing-responsive temperate phages. IMPORTANCEThe discovery of quorum-sensing responsive linear plasmid phages has transformed understanding of phage-bacterial interactions by demonstrating inter-domain chemical communication. To date, however, examples of quorum-sensing responsive phages have been sparse. The founding example of such a phage, {varphi}VP882, detects a chemical communication signal molecule called DPO that is produced by diverse bacterial species. We investigated whether a family of VP882-like phages might exist that detect and respond to DPO. We find that indeed, VP882-like phages reside in DPO-producing bacterial species isolated at different times and geographic locations, suggesting their wide circulation in the environment. This observation strengthens the evidence for the generality of phage-bacterial inter-domain chemical communication.

microbiology↗

bioRxiv2021

Pandemic Vibrio cholerae Acquired Competitive Traits from an Environmental Vibrio Species

BackgroundVibrio cholerae, the causative agent of cholera, is a human pathogen that thrives in estuarine environments. V. cholerae competes with neighboring microbes by the contact-dependent translocation of toxic effectors with the type VI secretion system (T6SS). Effector types are highly variable across V. cholerae strains, but all pandemic isolates encode the same set of distinct effectors. It is possible that acquisition of these effectors via horizontal gene transfer played a role in the development of pandemic V. cholerae. ResultsWe assessed the distribution of V. cholerae T6SS loci across multiple Vibrio species. We showed that the fish-pathogen V. anguillarum encodes all three V. cholerae core loci as well as two of the four additional auxiliary clusters. We further demonstrated that V. anguillarum shares T6SS effectors with V. cholerae, including every pandemic-associated V. cholerae effector. We identified a novel T6SS cluster (Accessory Aux1) that is widespread in V. anguillarum and encodes the pandemic V. cholerae effector TseL. We highlighted potential gene transfer events of Accessory Aux1 from V. anguillarum to V. cholerae. Finally, we showed that TseL from V. cholerae can be neutralized by the V. anguillarum Accessory Aux1 immunity protein and vice versa, indicating V. anguillarum as the donor of tseL to the V. cholerae species. ConclusionsV. anguillarum constitutes an environmental reservoir of pandemic-associated V. cholerae T6SS effectors. V. anguillarum and V. cholerae likely share an environmental niche, compete, and exchange T6SS effectors. Further, our findings highlight the fish as a potential reservoir of pandemic V. cholerae.

genomics↗

bioRxiv2019

Vibrio cholerae Type VI Secretion System Auxiliary Cluster 3 is a Pandemic-associated Mobile Genetic Element

All sequenced Vibrio cholerae isolates encode a contact-dependent type VI secretion system (T6SS) in three loci that terminate in a toxic effector and cognate immunity protein (E/I) pair, allowing for competitor killing and clonal expansion in aquatic environments and the host gut. Recent studies have demonstrated variability in the toxic effectors produced by different V. cholerae strains and the propensity for effector genes to undergo horizontal gene transfer. Here we demonstrate that a fourth cluster, auxiliary cluster 3 (Aux3), encoding the E/I pair tseH/tsiH, is located directly downstream from two putative recombinases and is flanked by repeat elements resembling att sites. Genomic analysis of 749 V. cholerae isolates, including both pandemic and environmental strains, revealed that Aux3 exists in two states: a [~]40 kb prophage-like element in nine environmental isolates and a [~]6 kb element in pandemic isolates. These findings indicate that Aux3 in pandemic V. cholerae is evolutionarily related to an environmental prophage-like element. In both states, Aux3 excises from the chromosome via site-specific recombination to form a circular product, likely priming the module for horizontal transfer. Finally, we show that Aux3 can integrate into the Aux3-naive chromosome in an integrase-dependent, site-specific manner. This highlights the potential of Aux3 to undergo horizontal transfer by a phage-like mechanism, which based on pandemic coincidence may confer currently unknown fitness advantages to the recipient V. cholerae cell. Significance StatementV. cholerae is a human pathogen that causes pandemics affecting 2.8 million people annually (1). The O1 El Tor lineage is responsible for the current pandemic. A subset of non-O1 strains cause cholera-like disease by producing the major virulence factors cholera toxin and toxin co-regulated pilus but fail to cause pandemics. The full set of V. cholerae pandemic factors is unknown. Here we describe the type VI secretion system (T6SS) Aux3 element as a largely pandemic-specific factor that is evolutionarily related to an environmental prophage-like element circulating in non-pathogenic strains. These findings shed light on V. cholerae T6SS evolution and indicate the Aux3 element as a pandemic-enriched mobile genetic element.

microbiology↗