Hormone receptors and the regulation of insect metamorphosis

Presented is a brief review of the role of ecdysteroid and juvenile hormone (JH) receptors in the regulation of insect larval molting and metamorphosis of the epidermis and the nervous system, using examples from Manduca sexta and Drosophila melanogaster. Ecdysteroids cause a molt by combining with the ecdysone receptor (EcR) and the ultraspiracle protein (both members of the steroid hormone receptor superfamily) to activate directly a number of regulatory genes whose products both repress ongoing gene expression and stimulate genes associated with the production of the new stage in a cascading fashion. The presence of the JH-JH receptor (JHR) ensures that the molt is to another larval stage. At metamorphosis in the absence of JH, a new isoform of EcR and some new ecdysteroid-induced regulatory factors appear in response to low ecdysteroid. The subsequent high ecdysteroid then can activate a new cascade, causing the pupal molt. Also, the quantity of the new EcR isoform in metamorphosing larval neurons during adult development is correlated with cell fate. The JHR found in larval tissues is a 29-kDa nuclear protein that specifically binds JH with high affinity and is dependent on the presence of JH during ecdysteroid rises for its continued synthesis. This JHR represents a new class of intranuclear hormone receptors since it has no known DNA-binding domains and has a discrete subnuclear localization different from that of the EcR. Its specific action is unknown.