methoprene and tebufenozide

Chitin synthase catalyzes chitin synthesis in the exoskeleton, tracheal system and gut during insect development. A chitin synthase 1 (CfCHS1) cDNA was identified and cloned from the spruce budworm, Choristoneura fumiferana. The CfCHS1 cDNA is 5,300 bp in length and codes a 1,564-amino acid protein with a molecular mass of 178 kDa. The deduced protein contains 16 transmembrane helixes in its domains A and C. The single copy CfCHS1 gene expressed during each of the larval molts from the 3rd to the 6th instar. The gene expressed highly and periodically in the epidermis during each of molts, whereas no transcripts were detected in the midgut and fat body. 20-hydroxyecdysone and the ecdysone agonist RH5992 suppressed CfCHS1 expression, whereas the juvenile hormone analog methoprene induced CfCHS1 expression. These results implicate that CfCHS1 is involved in the chitin synthase and new chitin formation during molting in the insect.

Topics: Amino Acid Sequence; Animals; Base Sequence; Chitin; Chitin Synthase; Cloning, Molecular; DNA, Complementary; Ecdysterone; Epidermis; Gene Expression Regulation, Developmental; Hydrazines; Insect Proteins; Larva; Methoprene; Molecular Sequence Data; Moths; Sequence Alignment

Ecdysone agonists are hormonally active insect growth regulators that disrupt development of pest insects and have potential for development as insecticides. Their effects have been particularly well-studied in Lepidoptera and Coleoptera, but significantly less is known about their effects on dipterans, particularly aquatic species. The potency of three ecdysone agonists on larvae of 3 mosquito species, Aedes aegypti, Anopheles gambiae, and Culex quinquefasciatus, was examined. Anopheles gambiae was the most susceptible species and Ae. aegypti was the most resistant species to the effects of the three compounds tested. Potency, in descending order, was RH-2485 > RH-5992 > RH-5849. Dose-response relationships were determined for the three agonists; RH-2485 was found to be the most effective endocrine disruptor against all three species. The observed biological effects of these compounds were similar to those reported for other insects, and mosquitoes initiated molting and apolysis but did not complete a molt. In some cases, mosquito larvae synthesized a new cuticle that appeared to be normally sclerotized but the larvae failed to ecdyse and shed the exuvium. These compounds may prove to be valuable insect growth regulators for control of mosquitoes to decrease the frequency of pathogen transmission to humans. Prospects for using these compounds to control mosquitoes in the field are discussed, along with possible impacts on non-target arthropods in mosquito habitats.

Topics: Animals; Culicidae; Dose-Response Relationship, Drug; Ecdysone; Hydrazines; Juvenile Hormones; Larva; Logistic Models; Methoprene

In the tobacco hornworm (Manduca sexta), vitellogenin (Vg), the major yolk protein precursor, and its mRNA are first detectable in the prepupal stage; and production of both can be enhanced by methoprene, a juvenile hormone (JH) analog. Competence to respond to methoprene is acquired after ecdysteroid-initiated commitment for metamorphosis. Here we show that acquisition of competence requires prior exposure to JH-II acid in addition to ecdysteroid. Application of 20-hydroxyecdysone or RH5992, an ecdysteroid analog, to isolated abdomens from feeding larvae (precommitment) results in exposure of the dorsal vessel (EDV), a sign of metamorphic commitment--but such abdomens do not make Vg in response to methoprene. However, injection of JH-II acid along with 20-hydroxyecdysone into isolated abdomens causes Vg production in response to methoprene. Methoprene acid similarly induces competence to respond to methoprene. Northern blot analysis confirmed that Vg transcripts are present in fat body only if isolated abdomens were pretreated with both ecdysteroid, and JH-II acid or methoprene acid. The latter two can induce competence even in precocious prepupae resulting from removal of the corpora allata (the glands that produce JH) from early penultimate larvae. JH-III acid and related metabolites such as farnesol, farnesoic acid, and methyl farnesoate do not induce competence. Hitherto, JH acids have been regarded as precursors or catabolites of JHs. Here we show for the first time that JH acid has a hormonal function that cannot be performed by JH itself.

Topics: Abdomen; Animals; Gene Expression Regulation, Developmental; Hemolymph; Hydrazines; Insect Hormones; Juvenile Hormones; Larva; Manduca; Metamorphosis, Biological; Methoprene; RNA, Messenger; Transcription, Genetic; Vitellogenins