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Mi-1-Mediated Aphid Resistance Involves Salicylic Acid and Mitogen-Activated Protein Kinase Signaling Cascades

June 2006 , Volume 19 , Number  6
Pages  655 - 664

Qi Li , 1 Qi-Guang Xie , 1 Jennifer Smith-Becker , 1 Duroy A. Navarre , 2 and Isgouhi Kaloshian 1

1Department of Nematology, University of California, Riverside, CA 92521, U.S.A.; 2Vegetable and Forage Crop Research Unit, USDA- Agricultural Research Service, Washington State University, Prosser, WA 99350, U.S.A.

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Accepted 5 February 2006.

The tomato Mi-1 gene confers resistance to root-knot nematodes (Meloidogyne spp.), potato aphids (Macrosiphum euphorbiae), and whiteflies (Bemisia tabaci and B. tabaci biotype B). Resistance to potato aphid is developmentally regulated and is not associated with induction of a hypersensitive response. The NahG transgene that eliminates endogenous salicylic acid (SA) was used to test the role of the SA signaling pathway in the resistance mediated by Mi-1 to potato aphids. Aphids survived longer on NahG tomato plants than on wild type. However, aphid reproduction was not affected on NahG tomato. Aphid resistance in Mi-1 NahG plants was completely abolished and the phenotype was successfully rescued by application of BTH (benzo(1,2,3)-thiaiazole-7-carbothioic acid S-methyl ester), indicating that the SA signaling pathway is an important component of Mi-1-mediated aphid resistance. Using virus-induced gene silencing, one or more mitogen-activated protein kinase (MAPK) cascades required for Mi-1-mediated aphid resistance were identified. Silencing plants for MAPK kinase (LeMKK2) and MAPKs (LeMPK2 and LeMPK1, or LeMPK3) resulted in attenuation of Mi-1-mediated aphid resistance. These results further demonstrate that resistance gene-mediated signaling events against piercing-sucking insects are similar to those against other plant pathogens.

Additional keywords: gene-for-gene resistance, resistance signaling.

© 2006 The American Phytopathological Society