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ABSTRACT:
PROVIDER: PRJNA883424 | ENA |
REPOSITORIES: ENA
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Project description:Complete genome assemblies of foodborne pathogens using MinION sequencing
| PRJNA498670 | ENA
Project description:Vibrio vulnificus causes severe necrotizing wound infections and life-threatening foodborne infections. While clinical isolates of V. vulnificus are well-established as human pathogens, the pathogenic mechanisms underlying the virulence of food-derived isolates, particularly in the case of wound infections, remain poorly understood. This study aimed to elucidate the pathogenic mechanisms of a highly virulent, seafood-derived V. vulnificus isolate. A molecular survey of 28 V. vulnificus isolates from Shenzhen identified four MARTX toxin types, with the D-type predominating (36%). We characterized a representative shrimp-derived isolate, Vv3, which carries a chromosomal D-type MARTX with an ACD-MCF-ABH-MCF effector architecture. Using a newly established mouse wound infection model, Vv3 induced 100% mortality within 12 hours, with high bacterial loads detected systemically. Pathological analysis revealed severe tissue damage at the infection site, marked by muscle necrosis, and significant distal organ damage. Strikingly, flow cytometry analysis of splenocytes showed a significant depletion of macrophages and lymphocytes, rather than a classic cytokine storm, which was supported by transcriptomic data. To dissect the molecular drivers underlying the pathogenicity of food-derived V. vulnificus, we generated isogenic toxin mutants. In vitro assays demonstrated that the MARTX toxin was the primary mediator of rapid cell death in both macrophages and epithelial cells. Deletion of the GD-rich repeat domain in the MARTX toxin (ΔrtxA-GD) significantly reduced cytotoxicity and allowed cells to maintain their morphology, while deletion of hemolysin (ΔvvhA) had a minor effect. Critically, In vivo mice wound infections indicated that MARTX-deficient mutants with or without deletion of vvhA is unable to cause mortality in mice. These results establish that the D-type MARTX toxin is the dominant virulence determinant in this foodborne isolate, driving mortality through a direct destruction of host cells. This study highlights the severe risk posed by foodborne V. vulnificus in wound exposures and informs that the GD-rich region serves as a potential target for intervention against V. vulnificus infection.
2025-09-22 | GSE308195 | GEO
Project description:A comparative genomic approach was used to identify large sequence polymorphisms among Mycobacterium avium isolates obtained from a variety of host species. DNA microarrays were used as a platform for comparing mycobacteria field isolates with the sequenced bovine isolate Mycobacterium avium subsp. paratuberculosis (Map) K10. ORFs were classified as present or divergent based on the relative fluorescent intensities of the experimental samples compared to Map K10 DNA. Map isolates cultured from cattle, bison, sheep, goat, avian, and human sources were hybridized to the Map microarray. Three large deletions were observed in the genomes of four Map isolates obtained from sheep and four clusters of ORFs homologous to sequences in the Mycobacterium avium subsp. avium (Maa) 104 genome were identified as being present in these isolates. One of these clusters encodes glycopeptidolipid biosynthesis enzymes. One of the Map sheep isolates had a genome profile similar to a group of Mycobacterium avium subsp. silvaticum (Mas) isolates which included four independent laboratory stocks of the organism traditionally identified as Maa strain 18. Genome diversity in Map appears to be mostly restricted to large sequence polymorphisms that are often associated with mobile genetic elements. Keywords: Comparative genomic hybridization
2007-04-27 | GSE7622 | GEO