The coat protein of Alfalfa mosaic virus interacts and interferes with the transcriptional activity of the bHLH transcription factor ILR3 promoting salicylic acid‐dependent defence signalling response. (8th May 2016)

• Record Type: Journal Article
• Authors: Aparicio, Frederic; Pallás, Vicente
• Is Part Of: Molecular plant pathology. Volume 18:Number 2(2017)
• Page Start: 173
• Page End: 186
• Publication Date: 2016-05-08
• Subjects: AMV -- coat protein -- nucleolus -- plant defense -- ROS -- transcription factors -- virus‐interactions; Plant diseases -- Molecular aspects -- Periodicals; Plant-pathogen relationships -- Molecular aspects -- Periodicals; 571.936
• DOI: 10.1111/mpp.12388
• Languages: English
• ISSNs: 1464-6722

Abstract

Summary: During virus infection, specific viral component–host factor interaction elicits the transcriptional reprogramming of diverse cellular pathways. Alfalfa mosaic virus (AMV) can establish a compatible interaction in tobacco and Arabidopsis hosts. We show that the coat protein (CP) of AMV interacts directly with transcription factor (TF) ILR3 of both species. ILR3 is a basic helix–loop–helix (bHLH) family member of TFs, previously proposed to participate in diverse metabolic pathways. ILR3 has been shown to regulate NEET in Arabidopsis, a critical protein in plant development, senescence, iron metabolism and reactive oxygen species (ROS) homeostasis. We show that the AMV CP–ILR3 interaction causes a fraction of this TF to relocate from the nucleus to the nucleolus. ROS, pathogenesis‐related protein 1 (PR1) mRNAs, salicylic acid (SA) and jasmonic acid (JA) contents are increased in healthy Arabidopsis loss‐of‐function ILR3 mutant (ilr3.2) plants, which implicates ILR3 in the regulation of plant defence responses. In AMV‐infected wild‐type (wt) plants, NEET expression is reduced slightly, but is induced significantly in ilr3.2 mutant plants. Furthermore, the accumulation of SA and JA is induced in Arabidopsis wt‐infected plants. AMV infection in ilr3.2 plants increases JA by over 10‐fold, and SA is reduced significantly, indicating an antagonist crosstalk effect. The accumulation levels of viral RNAs are decreased significantly in ilr3.2 mutants, but the virus can still systemically invade the plant. The AMV CP–ILR3 interaction may down‐regulate a host factor, NEET, leading to the activation of plant hormone responses to obtain a hormonal equilibrium state, where infection remains at a level that does not affect plant viability