Genetic analyses of the FRNK motif function of turnip mosaic virus uncover multiple and potentially interactive pathways of cross-protection
Journal
Molecular Plant-Microbe Interactions
Journal Volume
27
Journal Issue
9
Pages
944-955
Date Issued
2014
Author(s)
Kung Y.-J.
Lin P.-C.
Yeh S.-D.
Hong S.-F.
Chua N.-H.
Liu L.-Y.
Lin C.-P.
Huang Y.-H.
Wu H.-W.
Chen C.-C.
CHAN-PIN LIN
Abstract
Cross-protection triggered by a mild strain of virus acts as a prophylaxis to prevent subsequent infections by related viruses in plants; however, the underling mechanisms are not fully understood. Through mutagenesis, we isolated a mutant strain of Turnip mosaic virus (TuMV), named Tu-GK, that contains an Arg182Lys substitution in helper component-proteinase (HC-Pro(K)) that confers complete cross-protection against infection by a severe strain of TuMV in Nicotiana benthamiana, Arabidopsis thaliana Col-0, and the Arabidopsis dcl2-4/dcl4-1 double mutant defective in DICER-like ribonuclease (DCL)2/DCL4-mediated silencing. Our analyses showed that HC-Pro(K) loses the ability to interfere with microRNA pathways, although it retains a partial capability for RNA silencing suppression triggered by DCL. We further showed that Tu-GK infection triggers strong salicylic acid (SA)-dependent and SA-independent innate immunity responses. Our data suggest that DCL2/4-dependent and -independent RNA silencing pathways are involved, and may crosstalk with basal innate immunity pathways, in host defense and in cross-protection.
Type
journal article