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

Frontiers in Microbiology

Satyabrata Bag¹  Afsar Ali¹  Meer T. Alam¹  J. Glenn Morris Jr.²  Shrestha Sinha-Ray³ 

[1] Department of Environmental and Global Health, College of Public Health and Health Professions, University of Florida, Gainesville, FL, United States;Department of Medicine, School of Medicine, University of Florida, Gainesville, FL, United States;Department of Microbiology and Cell Science, College of Agricultural and Life Sciences, University of Florida, Gainesville, FL, United States;Emerging Pathogens Institute, University of Florida, Gainesville, FL, United States;

关键词: Vibrio cholerae;    chitin-induced natural transformation;    RS1-CTX-TLC prophages acquisition;    cholera toxin;    Haiti;    aquatic reservoirs;   

DOI  :  10.3389/fmicb.2019.02562

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown