|Coudron, Thomas - Tom|
|Wright Osment, Maureen|
Submitted to: Society For Experimental Biology And Medicine Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 6/21/2000
Publication Date: N/A
Citation: N/A Interpretive Summary:
Technical Abstract: Parasite venoms are potential sources of a wide diversity of new insect growth regulators. The venom of the parasite Euplectrus comstockii is unique in that it acts alone, and does not paralyze its host, but instead controls development in lepidopteran larvae by arresting molting. Molting arrestment consists of two responses - arrestment of apolysis and ecdysis, and arrestment of only ecdysis. Host response to the venom is dependent upon the host species, stage of development, and the venom dose. In vivo, arrestment activity persists in the hemolymph of the host for only 12 hours, whereas in vitro, venom incubated in buffer or hemolymph retains its original activity for greater than 24 hours, indicating that a non-humoral host factor is responsible for this inactivation. A 66 kDa protein isolated from Euplectrus venom arrests host molting. The presence of this protein in the hemolymph of parasitized larvae closely correlates with the arrestment activity. The integument from parasitized larvae cultured in vitro fails to produce new cuticle in response to 20-hydroxyecdysone, whereas nonparasitized integument cultured under the same conditions produces a normal cuticle. Similarly, injection of 20-hydroxyecdysone into parasitized larvae fails to override molting arrestment. Nonetheless, evidence for glycosylation of ecdysteroids has been found in the hemolymph of larvae parasitized by Euplectrus. The venom also changes host physiology by inducing the premature production of storage protein in permissive hosts. The induction of storage protein by the venom is a transcriptionally regulated event. Future studies are directed toward elucidating the mechanism by which the venom of Euplectrus comstockii arrests both apolysis and ecdysis in lepidopteran larvae.