Abstract

The currently accepted model of moult control in crustaceans relies entirely on the hypothesis that moult-inhibiting hormone (MIH) and crustacean hyperglycaemic hormone (CHH) repress ecdysteroid synthesis of the target tissue (Y-organ) only during intermoult, and that changes in synthesis and/or release of these neurohormones are central to moult control. To further refine this model, we investigated the biological activities of these neuropeptides in the crab Carcinus maenas, at the target tissue, receptor and cellular level by bioassay (inhibition of ecdysteroid synthesis), radioligand (receptor) binding assays, and second messenger (cGMP) assays, at defined stages of the moult cycle. To investigate possible moult cycle-related changes in neuropeptide biosynthesis, steady-state transcript levels of both neuropeptide mRNAs were measured by quantitative RT-PCR, and stored neuropeptide levels in the sinus gland were quantified during intermoult and premoult. The results show that the most important level of moult control lies within the signalling machinery of the target tissue, that expression and biosynthesis of both neuropeptides is constant during the moult cycle, and are not central to the currently accepted model of moult control.