Identification Of Related Genes Encoding Glycometabolism In The Cotton Bollworm, Helicoverpa Armigera

Environmental conditions are not always suitable for growth and development, and most insect species have evolved an adaptive strategy known as diapause to survive an unfavorable season. Diapause is a complex physiological and biochemical process accompanied by low metabolism, increased resistance and developmental arrest. Many evidences have been identified that hormone are key factors to regulate diapause. PTTH-ecdysone signaling is well-known that regulated pupal diapause. Changes of physiology and biochemistry on diapause have been widely studies, however, the molecular mechanisms are unclear. Thus, we try to answer why metabolic activity is suppressed during pupal diapause in the cotton bollworm, Helicoverpa armigera.Diapause results in low metabolic activity and a profound extension of insect lifespan. Here, we cloned Helicoverpa armigera Hexokinase(HK) gene, a gene that is critical for the developmental arrest of this species. HK expression and activity levels were significantly increased in nondiapause-destined pupae compared with those of diapause-destined pupae. Downregulation of HK activity reduced cell viability and delayed pupal development by reducing metabolic activity and increasing ROS activity, which suggests that HK is a key regulator of insect development. We then identified the transcription factors Har-CREB,-c-Myc, and-POU as specifically binding the Har-HK promoter and regulating its activity. Intriguingly, Har-POU and-c-Myc are specific transcription factors for HK expression, whereas Har-CREB is nonspecific. Furthermore, Har-POU and-c-Myc could respond to ecdysone, which is an upstream hormone. Therefore, low ecdysone levels in diapause-destined individuals lead to low Har-POU and-c-Myc expression levels, ultimately repressing Har-HK expression and inducing entry into diapause or lifespan extension.Mitochondria is a major place for energy metabolism. Previous studies have demonstrated that COX activity downregulates in diapause pupae, which indicate that mitochondrial activity is suppressed. But the molecular mechanism is unclear. Here, we show that HIF-1α expression is significantly increased in diapause-destined pupal brains compared to nondiapause-destined pupal brains and that HIF-1α negatively regulates mitochondrial biogenesis. HIF-1α mediates this effect by inhibiting c-Myc activity via proteasome-dependent degradation of c-Myc. The mitochondrial transcription factor A(TFAM), which encodes a key factor involved in mitochondrial transcription and mitochondrial DNA replication, is activated by the binding of c-Myc to the TFAM promoter, thereby inducing transcription. Loss of TFAM expression is a major factor contributing to reducing the mitochondrial activity. Thus, the HIF-1α-c-Myc-TFAM signaling pathway participates in the regulation of mitochondrial activity for insect diapause or lifespan extension.Insulin signaling regulates individual’ development via the regulation of energy metabolism. Many studies have demonstrated that insulin participates in the regulation of insect diapause. Here, we investigated InR and P-InR expression in diapause- and nondiapause-destined pupal brains, showed that InR and P-InR expression are significantly increased in diapause-destined individuals compared to nondiapause-destined individuals. The insulin activated P-ERK through P-InR. ROS can activate P-AKT and P-ERK by increased P-InR expression. Taken together, we demonstrated that ROS-P-InR-P-ERK signaling regulates pupal diapause by promoting proteasome activity to degrade target proteins.