Juvenile Hormone Induces Degeneration Of Flight Muscle Through Inhibiting Glycometabolism In The Parthenogenetic Winged Pea Aphid,Acyrthosiphon Pisum

Parthenogenetic winged aphids usually present a trade-off between flight and reproduction post eclosion.Newly emerged adults colonize a new host after flight with flight muscle gradually degenerated afterward,and subsequently promote their fecundity.While the causation of juvenile hormone(JH)and such degeneration have been tentatively established,more unambiguous supports are needed since the physiological mechanism underlies importing of nutrition-depended signaling remains unclear.Here,we present molecular validation and explore potential nutritional signaling pathway for JH mediated flight muscle degeneration in the pea aphid,Acyrthosiphon pisum.In view of transcriptome,glycometabolism and oxidative phosphorylation pathway are significantly inhibited in the methoprene induced degenerating flight muscle under starvation,which are also occurs in the nutrition-dependent degenerating flight muscle,compared with integral flight muscle treated with acetone.What is more,valinomycin microinjection mimics methoprene topical application under starvation.Transcriptional levels of key genes involving in JH sensitivity(Ap-met,Ap-Hsp83,Ap-importin and Ap-Nup358)and action,Ap-kr-h1,are up-regulated in the colonized winged A.pisum with degenerating flight muscle compared with aphids that have not yet been colonized.While,transcriptional level of key JH synthesis gene,Ap-jhamt,is relatively stable with the colonization process.In the meantime,the expression of Ap-jhamt is significantly down-regulated during starvation post eclosion.RNAi-Ap-jhamt or RNAi-Ap-met delays flight muscle degeneration.Transcriptional level of In R2 is down-regulated,and the phosphorylation levels of Akt and 4EBP are up-regulated with the colonization process.Wortmannin or rapamycin microinjection suppresses the transcription of Ap-jhamt and Ap-kr-h1 and delays flight muscle degeneration.RNAi-Ap-In R2 induces the high expression of Ap-jhamt,Ap-met and Ap-kr-h1,but is unable to induce obvious flight muscle degeneration.The current results indicate that JH induces the degeneration of flight muscle through inhibiting glycometabolism,which owing to drastic rise of JH sensitivity,and further demonstrate the key role of insulin/TOR pathway in importing nutrition signal to initiate such degeneration in the hemipterous aphids.