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Venom from the ectoparasitoid wasp Eulophus pennicornis disrupts host ecdysteroid production by regulating host prothoracic gland activity

2001; Wiley; Volume: 26; Issue: 3 Linguagem: Inglês

10.1046/j.0307-6962.2001.00240.x

1365-3032

Gay C. Marris, Robert J. Weaver, Julie Bell, John Edwards,

Entomological Studies and Ecology

Abstract. Attack by the ectoparasitoid Eulophus pennicornis Nees (Hymenoptera: Eulophidae) prevents larvae of Lacanobia oleracea L. (Lepidoptera: Noctuidae) from moulting. Prothoracic glands (PGs) excised from parasitized or artificially envenomated hosts show a reduced basal level of ecdysteroid release at a time when non‐parasitized caterpillars produce an ecdysteroid surge (48 h post moult to 5th stadium = penultimate stadium in non‐venomated hosts). By contrast, PGs from similarly parasitized or envenomated caterpillars release comparatively high levels of ecdysteroid at 120 h post‐moult. Temporary inactivation of PGs cannot be attributed solely to a parasitoid‐induced reduction in cell viability, and incubation in E. pennicornis venom in vitro does not exert any direct effect on either PG cell viability or ecdysteroid release. However, inactivated PGs are not stimulated by forskolin, which may indicate that the absence of the required pre‐moult ecdysteroid surge in developmentally arrested L. oleracea is due to insensitivity to a prothoracicotropic hormone. Even though parasitized caterpillars never moult, reversed‐phase HPLC separations and radioimmunoassay confirm that they produce active moulting hormone (20‐hydroxyecdysone) at 120 h post‐moult. These results suggest that E. pennicornis arrests host development through the indirect effects on their hosts' PGs. This effect is not achieved through the destruction of gland cells, but more likely reflects the interruption of an innate cycle in PG activity, such that they lose their ability to respond to a normal cue to produce an essential hormone peak at a crucial point in development.