We made single and combined mutations in ompU, ompT, and the two putative porin genes vca1008 and vc0972. The fitness of the strains was tested in vitro and in the infant mouse model of intestinal infection. We also studied the transcriptional induction of vca1008 in vitro and during mouse infection. We show that vca1008 is induced during infection and is necessary and sufficient (in the absence of ompU, ompT, and vc0972) for infection.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC451605 | PMC |
| http://dx.doi.org/10.1128/JB.186.15.5167-5171.2004 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
CsrA controls ToxR levels by increasing the stability and translation of mRNA.
mBio
December 2024
Department of Molecular Biosciences and LaMontagne Center for Infectious Diseases, The University of Texas at Austin, Austin, Texas, USA.
Intestinal colonization and virulence factor production in response to environmental cues is mediated through several regulatory factors in , including the highly conserved RNA-binding global regulatory protein CsrA. We have shown previously that CsrA increases synthesis of the virulence-associated transcription factor ToxR in response to specific amino acids (NRES) and is required for the virulence of in the infant mouse model of cholera. In this study, we mapped the 5' untranslated region (5' UTR) of and showed that CsrA can bind directly to an RNA sequence encompassing the 5' UTR, indicating that the regulation of ToxR levels by CsrA is direct.
View Article and Find Full Text PDFSeventh pandemic Vibrio choleare O1 El Tor strain is responsible for the on-going pandemic outbreak of cholera globally. This strain evolved from non-pathogenic V. cholerae by acquiring seventh pandemic gene (VC 2346), pandemic Islands (VSP1 and VSP2), pathogenicity islands (VP1 and VP2) and CTX prophage region.
View Article and Find Full Text PDFGenetic and mutational analysis of virulence traits and their modulation in an environmental toxigenic non-O1/non-O139 strain, VCE232.
Microbiology (Reading)
February 2022
Infectious Diseases and Immunology Division, CSIR - Indian Institute of Chemical Biology, Kolkata 700 032, India.
O1 and O139 isolates deploy cholera toxin (CT) and toxin-coregulated pilus (TCP) to cause the diarrhoeal disease cholera. The and genes encoding CT and TCP are part of two acquired genetic elements, the CTX phage and pathogenicity island-1 (VPI-1), respectively. ToxR and ToxT proteins are the key regulators of virulence genes of O1 and O139.
View Article and Find Full Text PDFOuter Membrane Vesicles of Vibrio cholerae Protect and Deliver Active Cholera Toxin to Host Cells via Porin-Dependent Uptake.
mBio
June 2021
Institute of Molecular Biosciences, University of Graz, Graz, Austria.
Outer membrane vesicles (OMVs) are an emerging research field due to their multifactorial composition and involvement in interspecies and intraspecies communication. Recent studies indicate that vesicle release by Gram-negative bacterial pathogens is increased during colonization, as exemplified by the facultative human pathogen Vibrio cholerae upon oral ingestion by the host. In this study, we investigate the fate of OMVs produced by the Gram-negative facultative pathogen V.
View Article and Find Full Text PDFOuter Membrane Vesiculation Facilitates Surface Exchange and In Vivo Adaptation of Vibrio cholerae.
Cell Host Microbe
February 2020
Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria; BioTechMed Graz, 8010 Graz, Austria. Electronic address:
Gram-negative bacteria release outer membrane vesicles into the external milieu to deliver effector molecules that alter the host and facilitate virulence. Vesicle formation is driven by phospholipid accumulation in the outer membrane and regulated by the phospholipid transporter VacJ/Yrb. We use the facultative human pathogen Vibrio cholerae to show that VacJ/Yrb is silenced early during mammalian infection, which stimulates vesiculation that expedites bacterial surface exchange and adaptation to the host environment.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!