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Journal of Virology, March 2008, p. 2477-2485, Vol. 82, No. 5
0022-538X/08/$08.00+0     doi:10.1128/JVI.01865-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Tobacco Mosaic Virus Replicase-Auxin/Indole Acetic Acid Protein Interactions: Reprogramming the Auxin Response Pathway To Enhance Virus Infection{triangledown}

Meenu S. Padmanabhan,1 Sabrina R. Kramer,1 Xiao Wang,1 and James N. Culver1,2*

Department of Cell Biology and Molecular Genetics, University of Maryland,1 Center for Biosystems Research, University of Maryland Biotechnology Institute, College Park, Maryland 207422

Received 24 August 2007/ Accepted 10 December 2007

The replicase protein of Tobacco mosaic virus (TMV) disrupts the localization and stability of interacting auxin/indole acetic acid (Aux/IAA) proteins in Arabidopsis, altering auxin-mediated gene regulation and promoting disease development (M. S. Padmanabhan, S. P. Goregaoker, S. Golem, H. Shiferaw, and J. N. Culver, J. Virol. 79:2549-2558, 2005). In this study, a similar replicase-Aux/IAA interaction affecting disease development was identified in tomato. The ability of the TMV replicase to interact with Aux/IAA proteins from diverse hosts suggests that these interactions contribute to the infection process. To examine the role of this interaction in virus pathogenicity, the replication and spread of a TMV mutant with a reduced ability to interact with specific Aux/IAA proteins were examined. Within young (4- to 6-week-old) leaf tissue, there were no significant differences in the abilities of Aux/IAA-interacting or -noninteracting viruses to replicate and spread. In contrast, in mature (10- to 12-week-old) leaf tissue, the inability to interact with specific Aux/IAA proteins correlated with a significant reduction in virus accumulation. Correspondingly, interacting Aux/IAA levels are significantly higher in older tissue and the overaccumulation of a degradation-resistant Aux/IAA protein reduced virus accumulation in young leaf tissue. Combined, these findings suggest that TMV replicase-Aux/IAA interactions selectively enhance virus pathogenicity in tissues where Aux/IAA proteins accumulate. We speculate that the virus disrupts Aux/IAA functions as a means to reprogram the cellular environment of older cells to one that is more compatible for virus replication and spread.

* Corresponding author. Mailing address: Center for Biosystems Research, University of Maryland Biotechnology Institute, College Park, MD 20742. Phone: (301) 405-2912. Fax: (301) 314-9075. E-mail: jculver{at}umd.edu

{triangledown} Published ahead of print on 19 December 2007.

Journal of Virology, March 2008, p. 2477-2485, Vol. 82, No. 5
0022-538X/08/$08.00+0     doi:10.1128/JVI.01865-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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