|Reed, Darcy - UNIV CALIF, DEPT ENTOMOL|
|Beckage, Nancy - UNIV CALIF, DEPT ENTOMOL|
Submitted to: Journal of Insect Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 10, 1997
Publication Date: N/A
Interpretive Summary: Development of environmentally compatible insect pest control strategies to reduce pesticide use requires knowledge of the biochemical and endocrine mechanisms involved in host suppression by natural enemies, such as parasites. We have shown that one of the mechanisms by which a braconid wasp, Cotesia congregata, suppresses lepidopteran host development involves prevention of release of the insect brain hormone required for molting. Furthermore, the ability of its target site, a steroid-producing endocrine gland, to respond to this brain hormone is suppressed. Such information will be useful in designing methods to isolate the inhibitory factor(s) and to test its ability to inhibit development of economically important lepidopteran pests.
Technical Abstract: The ability of brains from Cotesia congregata-parasitized Manduca sexta, 5th-instar larvae to stimulate ecdysteroid production in vitro was examined by dose-response analysis using prothoracic glands from day-2, unparasitized 5th-instar larvae. When compared for the first 7 days of the 5th instar to the ecdysiotropic activity in brains from unparasitized animals, the activity per brain was similar. However, analysis of the size distribution of ecdysiotropic peptides from brains of parasitized animals revealed a form present only in parasitized animals that was larger than the 29 kDa standard. This suggests that neuropeptide processing may be inhibited by insect parasitization. Furthermore, examination of the ability of the prothoracic glands from parasitized and unparasitized animals to respond to ecdysiotropic extracts revealed that glands from parasitized animals were much less responsive, even though these glands secreted quantities of immunoreactive ecdysteroids similar to their unparasitized counterparts for the first few days of the 5th instar. We suggest that the developmental arrest following parasitization of M. sexta by C. congregata may result from both an inhibition of prothoracicotropic hormone processing and the ability to respond to this neurohormone, and that this may be a general mechanism involving other neuropeptides.