Transcriptomic and Phenotypic Analysis Reveals New Functions for the Tat Pathway in Yersinia pseudotuberculosis.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
Heroven, Ann Kathrin
MetadataShow full item record
AbstractThe twin-arginine translocation (Tat) system mediates the secretion of folded proteins that are identified via an N-terminal signal peptide in bacteria, plants, and archaea. Tat systems are associated with virulence in many bacterial pathogens, and our previous studies revealed that Tat-deficient Yersinia pseudotuberculosis was severely attenuated for virulence. Aiming to identify Tat-dependent pathways and phenotypes of relevance for in vivo infection, we analyzed the global transcriptome of parental and ΔtatC mutant strains of Y. pseudotuberculosis during exponential and stationary growth at 26°C and 37°C. The most significant changes in the transcriptome of the ΔtatC mutant were seen at 26°C during stationary-phase growth, and these included the altered expression of genes related to virulence, stress responses, and metabolism. Subsequent phenotypic analysis based on these transcriptome changes revealed several novel Tat-dependent phenotypes, including decreased YadA expression, impaired growth under iron-limited and high-copper conditions, as well as acidic pH and SDS. Several functionally related Tat substrates were also verified to contribute to these phenotypes. Interestingly, the phenotypic defects observed in the Tat-deficient strain were generally more pronounced than those in mutants lacking the Tat substrate predicted to contribute to that specific function. Altogether, this provides new insight into the impact of Tat deficiency on in vivo fitness and survival/replication of Y. pseudotuberculosis during infection.
CitationTranscriptomic and Phenotypic Analysis Reveals New Functions for the Tat Pathway in Yersinia pseudotuberculosis. 2016, 198 (20):2876-86 J. Bacteriol.
AffiliationHelmholtz Centre for infection research, Inhoffenstr. 7, 38124 Braunschweig, Germany.
JournalJournal of bacteriology
The following license files are associated with this item:
- Creative Commons
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by-nc-sa/4.0/
- The Tat Substrate SufI Is Critical for the Ability of Yersinia pseudotuberculosis To Cause Systemic Infection.
- Authors: Avican U, Doruk T, Östberg Y, Fahlgren A, Forsberg Å
- Issue date: 2017 Apr
- The twin arginine translocation system is essential for virulence of Yersinia pseudotuberculosis.
- Authors: Lavander M, Ericsson SK, Bröms JE, Forsberg A
- Issue date: 2006 Mar
- Disruption of the NlpD lipoprotein of the plague pathogen Yersinia pestis affects iron acquisition and the activity of the twin-arginine translocation system.
- Authors: Tidhar A, Levy Y, Zauberman A, Vagima Y, Gur D, Aftalion M, Israeli O, Chitlaru T, Ariel N, Flashner Y, Zvi A, Mamroud E
- Issue date: 2019 Jun
- The role of the phoPQ operon in the pathogenesis of the fully virulent CO92 strain of Yersinia pestis and the IP32953 strain of Yersinia pseudotuberculosis.
- Authors: Bozue J, Mou S, Moody KL, Cote CK, Trevino S, Fritz D, Worsham P
- Issue date: 2011 Jun
- Contribution of the Twin Arginine Translocation system to the exoproteome of Pseudomonas aeruginosa.
- Authors: Ball G, Antelmann H, Imbert PR, Gimenez MR, Voulhoux R, Ize B
- Issue date: 2016 Jun 9