Control and biochemical nature of the ecdysteroidogenic pathway

Abstract

Molting is elicited by a critical titer of ecdysteroids that includes the principal molting hormone, 20-hydroxyecdysone (20E), and ecdysone (E), which is the precursor of 20E but also has morphogenetic roles of its own. The prothoracic glands are the predominate source of ecdysteroids, and the rate of synthesis of these polyhydroxylated sterols is critical for molting and metamorphosis. This review concerns three aspects of ecdysteroidogenesis: (a) how the brain neuropeptide prothoracicotropic hormone (PTTH) initiates a transductory cascade in cells of the prothoracic gland, which results in an increased rate of ecdysteroid biosynthesis (upregulation); (b) how the concentrations of 20E in the hemolymph feed back on the prothoracic gland to decrease rates of ecdysteroidogenesis (downregulation); and (c) how the prothoracic gland cells convert cholesterol to the precursor of E and then 20E, a series of reactions only now being understood because of the use of a combination of classical biochemistry and molecular genetics.