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Effects of parasitization of Trichoplusia ni by Chelonus sp.
Author(s) -
BÜHLER ADRIAN,
HANZLIK TERRY N.,
HAMMOCK BRUCE D.
Publication year - 1985
Publication title -
physiological entomology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.693
H-Index - 57
eISSN - 1365-3032
pISSN - 0307-6962
DOI - 10.1111/j.1365-3032.1985.tb00060.x
Subject(s) - trichoplusia , juvenile hormone , braconidae , biology , hemolymph , noctuidae , lepidoptera genitalia , parasitoid wasp , cabbage looper , parasitoid , endocrinology , medicine , zoology , botany , hormone , larva
. Parasitization of Trichoplusia ni (Huebner) (Lepidoptera: Noctuidae) by Chelonus sp. (Hymenoptera: Braconidae), an egg‐larval parasitoid, leads to precocious cocoon spinning of the host in the fourth (penultimate) stadium followed by parasitoid emergence from the prepupa. We have investigated the mechanism by which Chelonus sp. disrupts host development. The developing larva and fluids injected by the adult female separately from the egg, are not the source of these effects, but it remains a possibility that the teratocytes, originating from the trophamnion of the parasitoid egg, are responsible. The titre of the juvenile hormone esterase activity in the haemolymph of the parasitized fourth instar host is similar to that in the initial period of the final instar of normal T. ni , but lacks the postwandering peak of activity. The increased JHE activity leads to a reduced JH titre early in the fourth stadia. This indicates that disruption of host development occurs within 12h after apolysis to the fourth stadium, if not before. Anti‐juvenile hormone activity is not detected in extracts of parasitized T. ni. The morphological and behavioural changes associated with precocious development of the T. ni host are prevented by applications of juvenile hormone I, juvenile hormone II and the juvenoid, Ro 10–3108, but not juvenile hormone III and the juvenoid R 20458. However, these applications fail to prevent the onset of juvenile hormone esterase activity, another marker of precocious development. These observations indicate that simple anti‐juvenile hormone activity may not be the mechanism of disruption of host development. Development of the parasitoid is disrupted by application of Ro 10–3108 and juvenile hormones I, II and III, but timing of eclosion is only affected by application of juvenile hormone I, juvenile hormone II and Ro 10–3108. This observation may indicate a discrimination by the parasitoid between its own juvenile hormone III and the host's juvenile hormone II.