Hormonal Control of Metamorphosis in Insects

The metamorphosis of insects is regulated by systemic hormonal signals, which are controlled by neurohormones from the brain . Insect molting and metamorphosis are controlled by two effector hormones: the steroid 20-hydroxyecdysone (20E) and the lipid juvenile hormone (JH) 20E initiates and coordinates each molt (whether larva-to-larva, larva-to-pupa, or pupa-to- adult) and regulates the changes in gene expression that occur during metamorphosis. High levels of JH prevents the ecdysone-induced changes in gene expression that are necessary for metamorphosis. Thus, its presence during a larval molt ensures that the result of that molt is another larval instar, not a pupa or an adult.
The molting process is initiated in the brain, where neurosecretory cells release pro- thoracicotropic hormone (PTTH) in response to neural, hormonal, or environmental signals .PTTH is a peptide hormone with a molecular weight of approximately 40,000, and it stimulates the production of ecdysone by the prothoracic gland by activating the RTK (receptor tyrosine kinase) pathway in those cells . Ecdysone is modified in peripheral tissues to become the active molting hormone 20E. Each molt is initiated by one or more pulses of 20E. For a larval molt, the first pulse produces a small rise in the 20E concentration in the larval hemolymph and elicits a change in cellular commitment in the epidermis. A second, larger pulse of 20E initiates the differentiation events associated with molting. These pulses of 20E commit and stimulate the epidermal cells to synthesize enzymes that digest the old cuticle and synthesize a new one.

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