Fig. 1.

Schematic illustration of hormonal regulation in insect metamorphosis and oogenesis. 20E acts through EcR/USP to activate the transcription of 20E-early responsive genes E74, E75, Br-C, E93, and Ftz-f1 and initiate larval–pupal or nymphal–adult metamorphosis [14, 15, 19, 175, 176]. JH-Met/Tai receptor complex activates the transcription of primary JH-early responsive gene Kr-h1 [20, 21, 23, 28]. Kr-h1 prevents immature larvae from precocious larval–pupal metamorphosis by inhibiting Br-C expression in holometabolous insects [31, 32]. Kr-h1 also inhibits precocious adult metamorphosis by repressing E93 expression in both hemimetabolous and holometabolous insects [32–35]. In addition, Kr-h1 inhibits Spok expression in the prothoracic gland to inhibit ecdysone synthesis and prevent precocious metamorphosis [36, 37], while EcR suppresses JH biosynthesis in by inhibiting the expression of HMGR and JHAMT to ensure the onset of metamorphosis. In adults, JH exerts its vitellogenic role through Kr-h1 to promote insect vitellogenesis and oogenesis [10, 38, 39, 43]. 20E signaling cascade is evolutionarily conserved during metamorphosis and oogenesis across insect orders [9, 10, 16–18]