Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1081302 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Type VI secretion systems (T6SS) are widely distributed among Vibrio species, yet their roles in the coexistence of toxigenic and non- toxigenic strains remain unclear. Here, we report a novel orphan T6SS effector-immunity module, TseVs-TsiVs, primarily harbored by non- toxigenic Vibrio cholerae. TseVs exhibits robust vibriocidal activity, specifically targeting susceptible Vibrios (lacking TsiVs). TseVs forms dual-membrane, ion-selective pores that collapse Na⁺/K⁺ homeostasis, resulting in membrane depolarization and ATP depletion. Remarkably, non-Vibrio bacteria evade TseVs through proton motive force (PMF)-dependent resilience, uncovering a previously unrecognized immunity-independent defense strategy. Furthermore, tseVs+ non- toxigenic V. cholerae strains are globally distributed and have dominated in recent decades, highlighting TseVs’s ecological significance in Vibrio population dynamics. By linking TseVs’s bioenergetic assassination to Vibrio population shifts, we demonstrate how T6SS effectors shape microbial genetic diversity. Our findings suggest that TseVs represents a promising model for precision antimicrobial strategies, minimizing collateral damage to commensal microbiota.
2025-04-25 | GSE295209 | GEO
Project description:Pandemic and endemic strains of Vibrio cholerae arise from toxigenic conversion by the CTXφ bacteriophage, a process by which CTXφ infects non-toxigenic strains of V. cholerae. CTXφ encodes the cholera toxin, an enterotoxin responsible for the watery diarrhea associated with cholera infections. Despite the critical role of CTXφ during infections, signals that affect CTXφ-driven toxigenic conversion or expression of the CTXφ-encoded cholera toxin remain poorly characterized, particularly in the context of the gut mucosa. Here, we identify mucin polymers as potent regulators of CTXφ-driven pathogenicity in V. cholerae. Our results indicate that mucin-associated O-glycans block toxigenic conversion by CTXφ and suppress the expression of CTXφ-related virulence factors, including the toxin co-regulated pilus and cholera toxin, by interfering with the TcpP/ToxR/ToxT virulence pathway. By synthesizing individual mucin glycan structures de novo, we identify the Core 2 motif as the critical structure governing this virulence attenuation. Overall, our results highlight a novel mechanism by which mucins and their associated O-glycan structures affect CTXφ-mediated evolution and pathogenicity of V. cholerae, underscoring the potential regulatory power housed within mucus.
2022-12-01 | GSE213598 | GEO
Project description:In presence of high concentrations of L-arabinose, Vibrio cholerae enters into a non-proliferative state. In V. cholerae, when L-arabinose in present into the media, it is incorporated and metabolized through the galactose pathway. In the present datasets we show that in presence of L-arabinose, transposon insertions in the galactose pathway confer a resistance to the detrimental effect of L-arabinose.
2020-11-16 | E-MTAB-9747 | biostudies-arrayexpress
Project description:The sole gain of laterally acquired virulence genes does not fully explain the transition of environmental strains into human pathogens. To date, the specific molecular drivers and fitness trade-offs that enable some strains within a population to undergo this process remain enigmatic. Here, we describe a small RNA (sRNA) with a unique modular structure that shapes the evolution of toxigenic Vibrio cholerae, the agent of cholera. The sRNA comprises of a highly variable 5’ module located within the ompU ORF and a conserved 3’ one downstream from the gene. The bimodular nature of the OmpU-encoded sRNA (OueS) generates allelic variants that differentially contribute to the emergence of virulence potential in some strains and associated fitness trade-offs between human infection and environmental survival. Unlike environmental counterparts, the OueS allele from toxigenic strains controls phenotypes essential during host colonization: a) stringently inhibits biofilm formation by suppressing the iron-responsive sRNA RyhB, and b) confers resistance against intestinal bacteriophages by activating the CBASS phage defense system. Toxigenic OueS is also required for successful intestinal colonization and acts as a functional surrogate of the master virulence regulator ToxR, controlling over 84% of its regulome. On the other hand, strains encoding environmental alleles of OueS exhibit higher competitive fitness than those harboring toxigenic ones during colonization of natural reservoirs such as crustaceans (Artemia salina) and phytoplankton (Microcystis aeruginosa). These results uncover the fitness trade-offs between human infection and environmental survival and costs associated with pathogen emergence.
2026-04-03 | GSE272640 | GEO
Project description:The sole gain of laterally acquired virulence genes does not fully explain the transition of environmental strains into human pathogens. To date, the specific molecular drivers and fitness trade-offs that enable some strains within a population to undergo this process remain enigmatic. Here, we describe a small RNA (sRNA) with a unique modular structure that shapes the evolution of toxigenic Vibrio cholerae, the agent of cholera. The sRNA comprises of a highly variable 5’ module located within the ompU ORF and a conserved 3’ one downstream from the gene. The bimodular nature of the OmpU-encoded sRNA (OueS) generates allelic variants that differentially contribute to the emergence of virulence potential in some strains and associated fitness trade-offs between human infection and environmental survival. Unlike environmental counterparts, the OueS allele from toxigenic strains controls phenotypes essential during host colonization: a) stringently inhibits biofilm formation by suppressing the iron-responsive sRNA RyhB, and b) confers resistance against intestinal bacteriophages by activating the CBASS phage defense system. Toxigenic OueS is also required for successful intestinal colonization and acts as a functional surrogate of the master virulence regulator ToxR, controlling over 84% of its regulome. On the other hand, strains encoding environmental alleles of OueS exhibit higher competitive fitness than those harboring toxigenic ones during colonization of natural reservoirs such as crustaceans (Artemia salina) and phytoplankton (Microcystis aeruginosa). These results uncover the fitness trade-offs between human infection and environmental survival and costs associated with pathogen emergence.
2026-04-03 | GSE272767 | GEO
Project description:Investigation of whole genome gene expression level changes in a Vibrio cholerae O395N1 delta-nqrA-F mutant, compared to the wild-type strain. Total RNA recovered from wild-type cultures of VIbrio cholerae O395N1 and its nqrA-F mutant strain. Each chip measures the expression level of 3,835 genes from Vibrio cholerae O1 biovar eltor str. N16961 with twenty average probes/gene, with five-fold technical redundancy.
2014-04-01 | E-GEOD-56387 | biostudies-arrayexpress
Project description:We used RNA-seq to determine transcriptional profiles of whole guts or IPCs isolated from guts infected with wild type or type VI secretion system deficient Vibrio cholerae. We found significant differences between guts and progenitor cells infected wild type or type VI secretion system deficient Vibrio cholerae.
2019-08-21 | GSE136069 | GEO
Project description:We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process. C. elegans were exposed to Vibrio cholerae and E.coli then hybridization on Affymetrix microarray chips.
2011-12-02 | E-GEOD-34026 | biostudies-arrayexpress
Project description:Study of the effect of L-Arabinose on chromosomes replication forks progression in Vibrio cholerae. Processed wig.mat file.
2023-10-30 | E-MTAB-13450 | biostudies-arrayexpress