The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Gene Review

exoT  -  exoenzyme T

Pseudomonas aeruginosa PAO1

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of exoT

  • The exoT open reading frame, cloned into a T7 expression system, produced a 53-kDa protein in Escherichia coli, termed Exo53, which reacted to antisera against exoenzyme S. A histidine-tagged derivative of recombinant Exo53 possessed approximately 0.2% of the ADP-ribosyltransferase activity of recombinant ExoS [1].
  • RESULTS: For the cytotoxic strain, mutation of either exoU or exoT alone had little effect on virulence, whereas simultaneous mutation of both exoT and exoU or of exsA resulted in a significantly reduced capacity to cause corneal disease [2].
  • We mapped the coding single nucleotide polymorphisms in four toxin genes-exoS, exoT, exoU, and exoY-of the Pseudomonas aeruginosa type III secretion system among several clinical isolates [3].
  • With the addition of exoS and exoT to the molecular arsenal, questions concerning in vivo toxicity and target specificities of exoenzyme S can be directly addressed [4].

High impact information on exoT

  • Uncoupling Crk signal transduction by Pseudomonas exoenzyme T [5].
  • Clinical isolates that injure lung epithelium in vivo and that are cytotoxic in vitro possess exoT but lack exoS, suggesting that ExoS is not the cytotoxin responsible for the pathology and cell death measured in these assays [6].
  • Therefore, we have systematically deleted the genes for the three known type III effector molecules (exoS, exoT, and exoY) in P. aeruginosa PAO1 and assayed the effect of the deletions, both singly and in combination, on cytotoxicity in vitro and in vivo [7].
  • Complementation with exoT alone increased colonization ( approximately 3-log increase) and increased virulence to almost the same levels as wild-type or exoU-complemented infections [2].
  • One representative clone contained the open reading frame exoT; this open reading frame encoded a protein of 457 amino acids which showed 75% amino acid identity to ExoS [1].

Biological context of exoT

  • Inactivation of exoT in an allelic-replacement strain resulted in an Exo53-deficient phenotype without modifying the expression of ExoS [1].

Anatomical context of exoT


  1. Genetic relationship between the 53- and 49-kilodalton forms of exoenzyme S from Pseudomonas aeruginosa. Yahr, T.L., Barbieri, J.T., Frank, D.W. J. Bacteriol. (1996) [Pubmed]
  2. Contribution of ExsA-regulated factors to corneal infection by cytotoxic and invasive Pseudomonas aeruginosa in a murine scarification model. Lee, E.J., Cowell, B.A., Evans, D.J., Fleiszig, S.M. Invest. Ophthalmol. Vis. Sci. (2003) [Pubmed]
  3. Single-nucleotide-polymorphism mapping of the Pseudomonas aeruginosa type III secretion toxins for development of a diagnostic multiplex PCR system. Ajayi, T., Allmond, L.R., Sawa, T., Wiener-Kronish, J.P. J. Clin. Microbiol. (2003) [Pubmed]
  4. Genetic analysis of exoenzyme S expression by Pseudomonas aeruginosa. Goranson, J., Frank, D.W. FEMS Microbiol. Lett. (1996) [Pubmed]
  5. Uncoupling Crk signal transduction by Pseudomonas exoenzyme T. Deng, Q., Sun, J., Barbieri, J.T. J. Biol. Chem. (2005) [Pubmed]
  6. ExoU expression by Pseudomonas aeruginosa correlates with acute cytotoxicity and epithelial injury. Finck-Barbançon, V., Goranson, J., Zhu, L., Sawa, T., Wiener-Kronish, J.P., Fleiszig, S.M., Wu, C., Mende-Mueller, L., Frank, D.W. Mol. Microbiol. (1997) [Pubmed]
  7. Role of the type III secreted exoenzymes S, T, and Y in systemic spread of Pseudomonas aeruginosa PAO1 in vivo. Vance, R.E., Rietsch, A., Mekalanos, J.J. Infect. Immun. (2005) [Pubmed]
  8. Exoenzyme S shows selective ADP-ribosylation and GTPase-activating protein (GAP) activities towards small GTPases in vivo. Henriksson, M.L., Sundin, C., Jansson, A.L., Forsberg, A., Palmer, R.H., Hallberg, B. Biochem. J. (2002) [Pubmed]
  9. ADP-ribosylation by exoenzyme T of Pseudomonas aeruginosa induces an irreversible effect on the host cell cytoskeleton in vivo. Sundin, C., Hallberg, B., Forsberg, A. FEMS Microbiol. Lett. (2004) [Pubmed]
WikiGenes - Universities