New data will be discussed on the means by which the prothoracicotropic hormone (PTTH) of Manduca sexta stimulates the prothoracic glands to synthesize and release 3-dehydroecdysone. The process is initiated by PTTH-opening of a calcium channel leading to an increase in the amount and activity of a number of protein kinases, one of which has the capacity to enter the nucleus. The others, PKA and S6 kinase are utilized to phosphorylate S6 which is a protein constituent of the ribosome and has important roles in modulating protein synthesis, and in this case, for the purpose of stimulating ecdysteroidogenesis. How the prothoracic glands are turned off once the hemolymph ecdysteroid level has reached a peak was answered by demonstrating changes in the isoforms of ultraspiracle (usp) and the ecdysone receptor (EcR) which compose a dimer. The studies reveal changes in particular isoforms when the prothoracic glands are challenged both in vitro and in vivo. By 20-hydroxyecdysone (20E). Since ecdysteroids may also have a modulating role on the corpus allatum (source of juvenile hormone), a series of studies was conducted with the ecdysone receptor of the corpus allatum in vitro. The data showed that the isoform composition was specifically and reproducibly changed in the presence of 20E. There have been many reports in the literature of JH stimulating or inhibiting the prothoracic glands in vivo so that the rate of ecdysteroid synthesis is changed. This view, for the most part, was based on experiments in vivo and it was not proven unequivocally that JH affects the prothoracic glands directly. Our studies on the Manduca prothoracic glands indicate that it is indeed an indirect effect of JH on the prothoracic glands eliciting the modulation of ecdysteroidogenesis.

Index terms: molting, control of; second messengers; signal transduction; EcR (ecdysteroid receptor).