Little is known about the mechanism by which Yops, proteins that Yersinia inject into the cytosol of macrophage, cause downregulation of the inflammatory response and diseases such as the plague. Now it appears that Yops are the first bacterial member of a new family of ubiquitin-like proteases.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 12 print issues and online access
$209.00 per year
only $17.42 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
References
Orth K. et al. Disruption of Signaling by Yersinia Effector YopJ, a Ubiquitin-Like Protein Protease. Science 290, 1594–1597 (2000).
Cornelis, G.R. & Van Gijsegem, F. Assembly and function of type III secretory systems. Annu. Rev. Microbiol. 54, 735–774 (2000).
Nakajima R. & Brubaker, R.R. Association between virulence of Yersinia pestis and suppression of γ interferon and tumor necrosis factor α Infect. Immun. 61, 23–31 (1993).
Boland A. & Cornelis G.R. Role of YopP in suppression of tumor necrosis factor α release by macrophages during Yersinia infection. Infect. Immun. 66,1878–1884 (1998).
Schesser K., et al. The yopJ locus is required for Yersinia-mediated inhibition of NF-κB activation and cytokine expression: YopJ contains a eukaryotic SH2-like domain that is essential for its repressive activity. Mol. Microbiol. 28, 1067–1079 (1998).
Meijer, L.K, Schesser, K., Wolf-Watz H., Sassone-Corsi, P. & Petterson S. The bacterial protein YopJ abrogates multiple signal transduction pathways that converge on the transcription factor CREB. Cell Micro. 2, 231–238 (2000).
Palmer, L.E., Hobbie, S., Galan, J.E. & Bliska, J.B. YopJ of Yersinia pseudotuberculosis is required for the inhibition of macrophage TNF-α production and downregulation of the MAP kinases p38 and JNK. Mol. Microbiol. 27, 953–965 (1998).
Ruckdeschel, K. et al. Yersinia enterocolitica impairs activation of transcription factor NF-κB: involvement in the induction of programmed cell death and in the suppression of the macrophage tumor necrosis factor alpha production. J. Exp. Med. 187, 1069–1079 (1998).
Orth, K. et al. Inhibition of the mitogen-activated protein kinase kinase superfamily by a Yersinia effector. Science 285, 1920–1923 (1999).
Van den Ackerveken, G., Marois, E. & Bonas, U. Recognition of the bacterial avirulence protein AvrBs3 occurs inside the host plant cell. Cell 87,1307–1316 (1996).
Yeh, E.T.H., Gong, L. & Kamitani T. Ubiquitin-like proteins: new wines in new bottles. Gene 248, 1–14 (2000).
Palmer, L.E., Pancetti, A.R., Greenberg, S. & Bliska, J.B. YopJ of Yersinia spp is sufficient to cause downregulation of multiple mitogen-activated protein kinases in eukaryotic cells. Infect. Immun. 67, 708–716 (1999).
Mills, S.D. et al. Yersinia enterocolitica induces apoptosis in macrophages by a process requiring functional type III secretion and translocation mechanisms and involving YopP, presumably acting as an effector protein. Proc. Natl. Acad. Sci. U.S.A. 94, 12638–12643 (1997).
Monack, D.M., Mecsas, J., Bouley, D. & Falkow, S. Yersinia-induced apoptosis in vivo aids in the establishment of a systemic infection of mice. J.Exp Med. 188, 2127–2137 (1998).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Cornelis, G., Denecker, G. Yersinia lead SUMO attack. Nat Med 7, 21–23 (2001). https://doi.org/10.1038/83298
Issue Date:
DOI: https://doi.org/10.1038/83298