High MEK/ERK signalling is a key regulator of diapause maintenance in the cotton bollworm, Helicoverpa armigera

MEK/ERK signalling has been identified as a key factor that terminates diapause in Sarcophaga crassipalpis and Bombyx mori. Paradoxically, high p-MEK/p-ERK signalling induces diapause in pupae of the moth Helicoverpa armigera; however, the regulatory mechanism is unknown. In the present study, we show that p-MEK and p-ERK are elevated in the brain of diapause-destined pupae and suppression of MEK/ERK activity terminates diapause progress. Reactive oxygen species (ROS) activate MEK/ERK signalling, causing large-scale phosphorylation of downstream proteins. The levels of ubiquitin-conjugated proteins are also significantly reduced when ROS or p-ERK level decreased. Moreover, terminated diapause progress by 20-hydroxyecdysone injection significantly decreases p-MEK, p-ERK and phospho-ribosomal S6 kinase levels, while phospho-MAPK substrates and ubiquitin-conjugated protein levels increase. Our data demonstrate that high MEK/ERK signalling mediated by ROS promotes diapause maintenance via increasing phosphorylation and degradation of downstream substrates. The results of this study may provide important information for understanding the regulatory mechanisms during insect diapause.

Automated summary

The study reveals that reactive oxygen species activate MEK/ERK signaling pathway, leading to the maintenance of diapause state. Inhibiting MEK/ERK activity can terminate the progress of diapause.