Toxoneuron nigriceps bracovirus (TnBV) inhibits ecdysteroidogenesis in Heliothis virescens by the inactivation of TOR pathway

Toxoneuron nigriceps bracovirus (TnBV) inhibits ecdysteroidogenesis in Heliothis virescens by the inactivation of TOR pathway Introduction: Toxoneuron nigriceps is an endoparasitoid wasp belonging to Braconidae family, and its host is the tobacco budworm Heliothis virescens. Previous studies on this system have shown how parasitism induces major changes in the host physiology. Among them is the arrest of ecdysteroidogenesis due to the functional inactivation of prothoracic glands (PGs) in last instar larvae, and as consequence the prevention of pupation. The polydnavirus associated to T. nigriceps, TnBV, induces a complex syndrome that makes PGs of the host unable to respond to the stimulus of the prothoracicotropic hormone (PTTH), inducing a decrease of general protein synthesis and phosphorylation. Previous work proved that TOR signalling is involved in ecdysteroidogenesis of H. virescens. Here we demonstrate that one of the effects of parasitization is the alteration of this pathway. Methods: To evaluate the effect of parasitization, the ecdysteroid title was estimated by enzyme-immunoassay (EIA) and the level of phosphorylation of two targets of TOR (S6K and 4E-BP proteins) by western blot. These analyses were performed after incubation with PTTH of PGs from parasitized larvae. Moreover, a transcriptomic analysis of PGs from parasitized and non-parasitized larvae was performed. Results/Conclusion: Results showed that parasitization decreases the phosphorylation of 4E-BP and S6K and ecdysteroids level, even in the presence of PTTH stimulus. Besides, transcriptomes analysis highlighted viral genes expression in PGs and a downregulation of TOR pathway. These results suggest that some of TnBV genes expressed in PGs are potentially involved in block of ecdysteroidogenesis through the TOR pathway alteration.