English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Toxigenic  Vibrio cholerae  strains, including strains in serogroups O1 and O139 associated with the clinical disease cholera, are ubiquitous in aquatic reservoirs, including fresh, estuarine, and marine environments. Humans acquire cholera by consuming water and/or food contaminated with the microorganism. The genome of toxigenic  V. cholerae  harbors a cholera-toxin producing prophage (CT-prophage) encoding genes that promote expression of cholera toxin. The CT-prophage in  V. cholerae  is flanked by two satellite prophages, RS1 and TLC. Using cell surface appendages (TCP and/or MSHA pili),  V. cholerae  can sequentially acquire TLC, RS1, and CTX phages by transduction; the genome of each of these phages ultimately integrates into  V. cholerae’s  genome in a site-specific manner. Here, we showed that a non-toxigenic  V. cholerae  O1 biotype El Tor strain, lacking the entire RS1-CTX-TLC prophage complex (designated as RCT: R for RS1, C for CTX and T for TLC prophage, respectively), was able to acquire RCT from donor genomic DNA (gDNA) of a wild-type  V. cholerae  strain (E7946) via chitin-induced transformation. Moreover, we demonstrated that a chitin-induced transformant (designated as AAS111) harboring RCT was capable of producing cholera toxin. We also showed that  recA , rather than  xerC  and  xerD  recombinases, promoted the acquisition of RCT from donor gDNA by the recipient non-toxigenic  V. cholerae  strain. Our data document the existence of an alternative pathway by which a non-toxigenic  V. cholerae  O1 strain can transform to a toxigenic strain by using chitin induction. As chitin is an abundant natural carbon source in aquatic reservoirs where  V. cholerae  is present, chitin-induced transformation may be an important driver in the emergence of new toxigenic  V. cholerae  strains.

Conversion of a recA-Mediated Non-toxigenic Vibrio cholerae O1 Strain to a Toxigenic Strain Using Chitin-Induced Transformation