Submitted to: Archives of Insect Biochemistry and Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 20, 2004
Publication Date: August 5, 2005
Citation: Gelman, D.B., Gerling, D., Blackburn, M.B., Hu, J.S. 2005. Host-parasite interactions between whiteflies and their parasitoids. Archives of Insect Biochemistry and Physiology. 60:209-222.
Interpretive Summary: Whiteflies are serious pests of food, fiber and ornamental plants. These tiny insects damage plants by feeding on plant juices, transmitting pathogenic viruses and producing honeydew, a sweet sticky substance that supports the growth of sooty mold. The sweet potato whitefly (SPWF) and the greenhouse whitefly (GHWF) attack more than 500 different species of plants in both field and greenhouse settings, causing billions of dollars of damage in crop losses world-wide each year. For the last several decades, chemical pesticides have been the preferred method for controlling whiteflies. Tiny wasp parasites in addition to being useful as biological control agents could contribute to the development of new biopesticides (compounds that would kill insects without harming other living things), if only the complex mechanisms by which they manipulate their hosts' physiology and biochemistry were well-understood. Unfortunately, there is very little information available in this area of research. Here we describe interactions that we have observed in four whitefly-parasite systems. Our results show that parasites inject or produce substances that interfere with whitefly immunity, that stop whitefly development, and that cause the whitefly to come out of hibernation months before the normal time. Results should be useful to other scientists, and should help to identify compounds that would be useful in the productions of biopesticides.
Little information is available concerning the physiological and biochemical interactions between whiteflies and their parasitoids. Interactions between aphelinid parasitoids and their aleyrodid hosts in four host-parasite systems: B. tabaci/E. formosa, T. vaporariorum/E. formosa, B. tabaci/E. mundus and T. lauri/E. scapeata are described. In the absence of polydanvirus and teratocytes, these parasitoids must inject and/or produce compounds that interfere with the host immune response and which manipulate host development to suit their own needs. Eretmocerus larvae only penetrated 4th instar B. tabaci nymphs. A pre-penetrating E. mundus first instar induced developmental arrest in its host, and upon penetration, stimulates its host to produce a capsule (epidermal in origin) in which the parasitoid larva develops. T. vaporariorum and B. tabaci parasitized by E. formosa also undergo development arrest. In these systems, the site of parasitoid oviposition depended on the host species, i.e., within or pressing into the ventral ganglion in T. vaporariorum and at various locations in B. tabaci. E. formosa's final larval molt is cued by the onset of adult development in its host. The T. lauri/E. scapeata system is one in which host and parasitoid diapause during most of the year. Most parasitized whiteflies broke diapause and began to develop two months earlier than unparasitized whiteflies. A small number of whiteflies swelled and exhibited parasitoid emergence holes in fall and winter. It appears, then, that E. scapeata can induce diapause break in its whitefly host.