Polydnaviruses are obligate viral symbionts of Ichneumonid and Braconid wasps, which exclusively attack the larval stages of their lepidopteran hosts. These viruses are injected by females during oviposition and selectively infect several host tissues, through the expression of viral genes without undergoing any replication events, which eventually results in host physiology manipulation, altering the neuroendocrine balance. Toxoneuron nigriceps bracovirus (TnBV) is associated to Toxoneuron nigriceps (Hymenoptera: Braconidae), the endoparasitoid wasp of Heliothis virescens (Lepidoptera: Noctuidae). Previous studies showed that H. virescens parasitized by T. nigriceps has a normal development up to the last larval instar, but fail to pupate, due to the arrest of ecdysteroidogenesis. Indeed, the main target tissues of TnBV gene expression are the prothoracic glands (PGs), responsible for the production and secretion of ecdysone, the molting hormone, following the prothoracicotropic hormone (PTTH) stimulus. TnBV induces a functional inactivation of PGs, making them not responsive to the PTTH stimulus, resulting in a considerable decrease of ecdysone levels. In H. virescens we previously investigated the involvement of PI3K/Akt/TOR pathway in ecdysteroidogenesis. Here, we showed that this cellular signaling is one of the targets of TnBV infection. Results of western blot and enzyme immunoassay demonstrated that parasitization inhibits the ecdysteroidogenesis and the phosphorylation of two targets of TOR (4E-BP and S6K), despite the stimulation of PTTH contained in the brain extract. Moreover, using a transcriptomic approach, we identified the viral genes selectively expressed in PGs of parasitized last instar larvae and observed lower expression levels of genes involved in PI3K/Akt/TOR pathway. The down-regulation of several genes of the TOR pathway (tor, 4e-bp and s6k) in PGs of parasitized larvae was confirmed by qRT-PCR, supporting the hypothesis of TnBV involvement in blocking ecdysteroidogenesis, at least in part through the alteration of the TOR pathway at the transcriptional level.
The expression of Toxoneuron nigriceps bracovirus (TnBV) genes induces the inhibition of TOR pathway gene transcription in Heliothis virescens prothoracic glands
Rosanna Salvia;Andrea Scala;Carmen Scieuzo;Marisa Nardiello;Donatella Farina;Sabino Aurelio Bufo;Patrizia Falabella
2018-01-01
Abstract
Polydnaviruses are obligate viral symbionts of Ichneumonid and Braconid wasps, which exclusively attack the larval stages of their lepidopteran hosts. These viruses are injected by females during oviposition and selectively infect several host tissues, through the expression of viral genes without undergoing any replication events, which eventually results in host physiology manipulation, altering the neuroendocrine balance. Toxoneuron nigriceps bracovirus (TnBV) is associated to Toxoneuron nigriceps (Hymenoptera: Braconidae), the endoparasitoid wasp of Heliothis virescens (Lepidoptera: Noctuidae). Previous studies showed that H. virescens parasitized by T. nigriceps has a normal development up to the last larval instar, but fail to pupate, due to the arrest of ecdysteroidogenesis. Indeed, the main target tissues of TnBV gene expression are the prothoracic glands (PGs), responsible for the production and secretion of ecdysone, the molting hormone, following the prothoracicotropic hormone (PTTH) stimulus. TnBV induces a functional inactivation of PGs, making them not responsive to the PTTH stimulus, resulting in a considerable decrease of ecdysone levels. In H. virescens we previously investigated the involvement of PI3K/Akt/TOR pathway in ecdysteroidogenesis. Here, we showed that this cellular signaling is one of the targets of TnBV infection. Results of western blot and enzyme immunoassay demonstrated that parasitization inhibits the ecdysteroidogenesis and the phosphorylation of two targets of TOR (4E-BP and S6K), despite the stimulation of PTTH contained in the brain extract. Moreover, using a transcriptomic approach, we identified the viral genes selectively expressed in PGs of parasitized last instar larvae and observed lower expression levels of genes involved in PI3K/Akt/TOR pathway. The down-regulation of several genes of the TOR pathway (tor, 4e-bp and s6k) in PGs of parasitized larvae was confirmed by qRT-PCR, supporting the hypothesis of TnBV involvement in blocking ecdysteroidogenesis, at least in part through the alteration of the TOR pathway at the transcriptional level.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
