Interaction of the Tobacco mosaic virus replicase protein with a NAC domain transcription factor is associated with the suppression of systemic host defenses.

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TitleInteraction of the Tobacco mosaic virus replicase protein with a NAC domain transcription factor is associated with the suppression of systemic host defenses.
Publication TypeJournal Article
Year of Publication2009
AuthorsWang, X, Goregaoker, SP, Culver, JN
JournalJ Virol
Volume83
Issue19
Pagination9720-30
Date Published2009 Oct
ISSN1098-5514
KeywordsArabidopsis, Green Fluorescent Proteins, Immunoprecipitation, Models, Genetic, Plants, Genetically Modified, Proteasome Endopeptidase Complex, Protein Structure, Tertiary, Reverse Transcriptase Polymerase Chain Reaction, RNA Replicase, Salicylic Acid, Tobacco Mosaic Virus, Transcription Factors, Transcriptional Activation, Transgenes, Two-Hybrid System Techniques
Abstract

An interaction between the helicase domain of the Tobacco mosaic virus (TMV) 126-/183-kDa replicase protein(s) and the Arabidopsis thaliana NAC domain transcription factor ATAF2 was identified via yeast two-hybrid and in planta immunoprecipitation assays. ATAF2 is transcriptionally induced in response to TMV infection, and its overexpression significantly reduces virus accumulation. Proteasome inhibition studies suggest that ATAF2 is targeted for degradation during virus infection. The transcriptional activity of known defense-associated marker genes PR1, PR2, and PDF1.2 significantly increase within transgenic plants overexpressing ATAF2. In contrast, these marker genes have reduced transcript levels in ATAF2 knockout or repressor plant lines. Thus, ATAF2 appears to function in the regulation of host basal defense responses. In response to TMV infections, ATAF2 and PR1 display increased transcript accumulations in inoculated tissues but not in systemically infected tissues. ATAF2 and PR1 transcript levels also increase in response to salicylic acid treatment. However, the salicylic acid treatment of systemically infected tissues did not produce a similar increase in either ATAF2 or PR1 transcripts, suggesting that host defense responses are attenuated during systemic virus invasion. Similarly, noninfected ATAF2 knockout or ATAF2 repressor lines display reduced levels of PR1 transcripts when treated with salicylic acid. Taken together, these findings suggest that the replicase-ATAF2 interaction suppresses basal host defenses as a means to promote systemic virus accumulation.

DOI10.1128/JVI.00941-09
Alternate JournalJ. Virol.
PubMed ID19625399
PubMed Central IDPMC2748025