QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online December 9, 2005
doi: 10.1242/10.1242/jcs.02709

This Article Figures Only Full Text Full Text (PDF) Supplementary Material Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Molestina, R. E. Articles by Sinai, A. P. Search for Related Content PubMed PubMed Citation Articles by Molestina, R. E. Articles by Sinai, A. P. Social Bookmarking                         What's this?

Host and parasite-derived IKK activities direct distinct temporal phases of NF-B activation and target gene expression following Toxoplasma gondii infection

Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky College of Medicine, Lexington, KY 40536, USA

^* Author for correspondence (e-mail: sinai{at}uky.edu)

Accepted 22 September 2005

Activation of NF-B by the intracellular pathogen Toxoplasma gondii is associated with the localization of phosphorylated IB to the parasitophorous vacuole membrane (PVM). This is mediated by a parasite-derived IB kinase (TgIKK) activity and is independent of host IKK function. In the present study, we examined the roles of host IKK and parasite-derived TgIKK on the temporal modulation of NF-B activation. Despite the presence of TgIKK activity at the PVM, nuclear translocation of NF-B and subsequent gene expression exhibited a requirement for the host IKK complex. A detailed kinetic analysis of NF-B activation revealed a biphasic, hierarchical and temporally regulated response. We propose a novel paradigm for the modulation of NF-B-dependent gene expression by T. gondii that involves both the host IKK complex and TgIKK activity at different phases of infection. Thus, T. gondii effectively alters gene expression in a temporal dimension by exploiting the NF-B signaling machinery and subsequently rewiring the activation circuits of the infected host cell.

Key words: Toxoplasma gondii, IKK, IB, NF-B

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				M. M. Nelson, A. R. Jones, J. C. Carmen, A. P. Sinai, R. Burchmore, and J. M. Wastling Modulation of the Host Cell Proteome by the Intracellular Apicomplexan Parasite Toxoplasma gondii Infect. Immun., February 1, 2008; 76(2): 828 - 844. [Abstract] [Full Text] [PDF]

				R. K. Herman, R. E. Molestina, A. P. Sinai, and D. K. Howe The Apicomplexan Pathogen Neospora caninum Inhibits Host Cell Apoptosis in the Absence of Discernible NF-{kappa}B Activation Infect. Immun., September 1, 2007; 75(9): 4255 - 4262. [Abstract] [Full Text] [PDF]

				V. B. Carruthers and Y. Suzuki Effects of Toxoplasma gondii Infection on the Brain Schizophr Bull, May 1, 2007; 33(3): 745 - 751. [Abstract] [Full Text] [PDF]

				A. E. Fouts and J. C. Boothroyd Infection with Toxoplasma gondii Bradyzoites Has a Diminished Impact on Host Transcript Levels Relative to Tachyzoite Infection Infect. Immun., February 1, 2007; 75(2): 634 - 642. [Abstract] [Full Text] [PDF]