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ARS Home » Pacific West Area » Parlier, California » San Joaquin Valley Agricultural Sciences Center » Crop Diseases, Pests and Genetics Research » Research » Publications at this Location » Publication #182068


item Backus, Elaine

Submitted to: International Auchenorrhyncha Congress
Publication Type: Proceedings
Publication Acceptance Date: 6/15/2005
Publication Date: 8/7/2005
Citation: Ranger, C.M., Backus, E.A. 2005. Cell-rupture feeding by empoasca spp.: how it causes hopperburn and plants defend against it. Proceedings of the 12th. International Auchenorrhyncha Congress. p.S-5-6.

Interpretive Summary: Hopperburn is a noninfectious plant disease attributed to the direct feeding damage caused by Empoasca spp. leafhoppers (Cicadellidae: Typhlocybinae). The work described in this proceedings paper shows exactly which feeding strategies and tactics cause hopperburn symptoms, and how certain plants can deter those types of feeding. Some host plants stimulate the insects to switch their feeding tactic to a less-damaging one. Others deter feeding via glandular trichomes which secrete nonvolatile fatty acides that act as behavioral deterrents. Knowledge of how feeding causes damage has allowed crop breeding companies to select plants for their ability to prevent feeding, ultimately leading to resistant crop varieties.

Technical Abstract: Hopperburn is a noninfectious plant disease attributed to the direct feeding damage caused by Empoasca spp. leafhoppers (Cicadellidae: Typhlocybinae). Cell rupturing is the characteristic feeding strategy employed by all Empoasca spp. (Backus et al. 2005). Electrical penetration graph monitoring determined three different stylet penetration tactics comprise the cell rupturing strategy, namely, lacerate-and-sip, lacerate-and-flush, and lance-and-ingest. While all Empoasca spp. possess the same repertoire, variations of the tactics and the tissues in which they are performed influence whether or not the hopperburn cascade will be initiated. Empoasca salivary components amplify the severity of the wound response first initiated by mechanical damage. Thus, initiation of the cascade of plant physiological events that cause hopperburn is termed a saliva-enhanced wound response. The combination of mechanical damage and salivary stimuli results in localized necrosis within probed regions, enlargement and proliferation of phloem parenchyma and vascular cambial cells. Vascular bundles become disorganized, collapsed, and constricted, resulting in an accumulation of photoassimilates in the leaves. Plants can successfully defend themselves against hopperburn by altering the repertoire of Empoasca feeding tactics. Elevated healing/ compensatory responses to mechanical and salivary factors can also minimize hopperburn symptoms.