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Genetic Analyses of the FRNK Motif Function of Turnip mosaic virus Uncover Multiple and Potentially Interactive Pathways of Cross-Protection

September 2014 , Volume 27 , Number  9
Pages  944 - 955

Yi-Jung Kung,1,2 Pin-Chun Lin,3 Shyi-Dong Yeh,2,4 Syuan-Fei Hong,5 Nam-Hai Chua,1 Li-Yu Liu,6 Chan-Pin Lin,3,7 Yu-Hsin Huang,3,7 Hui-Wen Wu,1 Chin-Chih Chen,8 and Shih-Shun Lin3,9,10

1The Plant Molecular Biology, The Rockefeller University, 1230 York Ave, New York 10065, U.S.A.; 2Department of Plant Pathology, National Chung-Hsing University, 250 Kao-Kung Rd., Taichung, Taiwan; 3Institute of Biotechnology, National Taiwan University, 81, Chang-Xing St., Taipei, Taiwan; 4NCHU-UCD Plant and Food Biotechnology Center, National Chung-Hsing University, Taichung, Taiwan; 5Department of Horticulture and Landscape Architecture, 6Department of Agronomy, and 7Department of Plant Pathology and Microbiology, National Taiwan University, 1, Sec 4, Roosevelt Rd., Taipei, Taiwan; 8Division of Plant Pathology, Agricultural Research Institute, Wu-Feng, Taichung Taiwan; 9Genome and Systems Biology Degree Program, National Taiwan University, Taipei, Taiwan; 10Agricultural Biotechnology Research Center, Academia Sinica, 128 Academia Rd, Sec. 2, Taipei, Taiwan

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Accepted 25 April 2014.

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-ProK) 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-ProK 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.

© 2014 The American Phytopathological Society