Aphid feeding is dependent upon the salivary gland to enable proper feeding by secreting saliva that contains bioactive agents that mitigate the plant response to tissue damage resulting from feeding. Further, the aphid salivary gland is the organ responsible for secreting ‘gel’ and watery saliva that form the stylet sheath and facilitate enzymatic food digestion, respectively. The formation of the styelet sheath is critical for feeding on the nutrient-rich phloem of plant tissue and ablation of stylet sheaths correspond with reduced phloem feeding. This suggests the salivary gland may represent a target tissue for inducing feeding cessation and/or toxicity that is distinctly different from commercialized neurotoxic insecticides. Therefore, we aimed to directly test the hypothesis that pharmacological inhibition of inward rectifier potassium (Kir) channels would result in salivary gland failure and reduced sap ingestion by the cotton aphid, Aphis gossypii. The insect specific Kir inhibitors VU041 and VU590 reduced the length of the salivary sheath in a concentration dependent manner, indicating that the secretory activity of the salivary gland is reduced by Kir inhibition. Next, we employed the electrical penetration graph (EPG) technique to measure the impact Kir inhibition has to aphid sap feeding and feeding biology. Data show that foliar application of VU041 eliminated the E1 and E2 phases (phloem feeding) in all aphids studied, which corresponds to the observed reduced sheath formation. Contact exposure to VU041 after foliar applications was found to be toxic to A. gossypii at 72- and 96-hours post-infestation, indicating mortality is likely a result of starvation and not acute toxicity. Further, VU041 exposure significantly altered the feeding behavior of aphids by significantly reducing the time to first probe, the time spent in each probe, and the total probe duration. This change in behavior is toxicologically relevant for plant-virus interactions and thus, the influence of VU041 to reduce acquisition or transmission of phloem-restricted viruses was determined and will be discussed. These data suggest Kir channels are critical for proper function of aphid salivary glands and the reduced plant feeding justifies future work in developing salivary gland Kir channels as novel mechanism aphicides. Furthermore, products like VU041 would add to a very minor arsenal of compounds that simultaneously reduce vector abundance and alter feeding behavior.

Developing novel mechanism insecticides to inhibit feeding and vectorial capacity of the cotton aphid, Aphis gossypii

2019 Fall National Meeting

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