Poster: Signaling, long distance
Abs #
452: Deciphering the roles of ethylene and jasmonic acid in maize insect defense signaling
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Presenter: |
Harfouche, Antoine L, alh283@ra.msstate.edu |
Authors | Harfouche, Antoine L (A) Shivaji, Renuka (A) Lopez, Lorena (A) Williams, Paul W (B) Luthe, Dawn S (A) | | Affiliations: |
(A): Mississippi State University Department of Biochemistry and Molecular Biology
(B): USDA, ARS, Corn Host Plant Resistance Unit
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Our lab is attempting to decipher signaling pathways during plant-insect interactions in maize. Inhibitors of hormone synthesis and perception were used to determine if ethylene and jasmonic acid (JA) regulate the accumulation of a 33-kD cysteine proteinase (Mir1-CP), a defense protease that accumulates in response to caterpillar feeding in maize genotypes resistant to feeding by fall armyworm larvae. When whorls were treated with ethylene inhibitors, they accumulated reduced amounts of Mir1-CP and exhibited increased feeding damage. In addition, larvae reared on these tissues were significantly larger than those feeding on control plants and immunogold labeling showed fewer gold particles in the muscle connective tissues of the larval midgut. However, no changes in the expression of the mRNA (mir1) encoding Mir1-CP or the ethylene response gene XET were detected by RT-PCR. To determine the role of the octadecanoid signaling pathway in maize, plants were also treated with JA and ibuprofen, which inhibits lipoxygenase (LOX9) that catalyzes the rate-limiting step in JA biosynthesis. Semi-quantitative RT-PCR indicated that the expression of mir1 and LOX9 mRNAs increase in response to JA. Bioassays indicated that there was less feeding damage and larvae were smaller when they were reared on JA-treated plants. Larvae fed on plants treated with ibuprofen exhibited more feeding damage and the larvae were larger. These data suggest that both ethylene and JA signaling are required for resistance. Hydrogen peroxide detection on mechanically wounded or insect infested plants indicated that none of the ethylene and JA inhibitors or combinations of inhibitors prevented its production, suggesting that reactive oxygen species is upstream or independent of JA and ethylene signaling.
