Regulation of ecdysteroidogenesis and development in Heliothis virescens (Lepidoptera: Noctuidae) by the target of rapamycin TOR

Introduction: Molting in insects is regulated by endocrine changes that occurs at the end of an instar. The prothoracicotropic hormone (PTTH) is the stimulator of ecdysteroidogenesis in prothoracic glands (PGs). Recent studies showed that PI3K/Akt signaling and, specifically, TOR (Target of Rapamycin) pathway is involved in ecdysteroidogenesis. TOR is a serine-threonine kinase involved in several anabolic cellular processes, and the alteration of this pathway has been observed in numerous human diseases. Methods: To analyze the involvement of TOR signaling in Heliothis virescens PGs ecdysteroidogenesis, two different approaches were used. In vitro, the ecdysteroid titer was evaluated by enzyme-immunoassay (EIA) and the level of phosphorylation of two targets of TOR (S6K and 4E-BP proteins) was evaluated by western blot. These analyses were performed after prothoracic glands incubation with PTTH and/or Rapamycin, the specific inhibitor of TOR. In vivo, larvae of different instars were fed on diet treated with Rapamycin at various concentrations. Results/Conclusion: Results showed that PTTH increases the phosphorylation of 4E-BP and S6K and ecdysteroids level and that Rapamycin inhibits all of these processes. This suggests that TOR signaling is involved in PTTH-stimulated ecdysteroidogenesis by PGs in this model. Moreover, feeding on Rapamycin delays the growth rate, the onset of molt and implicate high mortality rate. Rapamycin also suppresses the growth of the PGs and the ecdysone production. Results obtained in vitro and in vivo underlines the involvement of TOR signaling in ecdysteroidogenesis and its important role in systemic growth.