Meeting Abstract

81.3  Tuesday, Jan. 6  Regulation of ecdysteroidogenesis in the decapod molting gland: a new synthesis COVI, J.A.*; MYKLES, D.L.; Colorado State Univ.; Colorado State Univ. joseph.covi@colostate.edu

Biochemical, physiological, and structural changes associated with molting in decapod crustaceans are orchestrated by ecdysteroids, and factors that inhibit the production of these polyhydroxylated steroids by the molting gland (Y-organ) ultimately regulate the molting cycle. The neuropeptide, molt inhibiting hormone (MIH), is the primary endocrine factor in control of ecdysteroidogenesis during intermolt. However, the signaling pathway activated by MIH remains a subject of controversy. From a broadly comparative perspective, data support the involvement of both cAMP and cGMP in MIH signaling. Differences among species in responsiveness of the Y-organ to specific pharmacological treatments offer insight into both the core and flexible components of neuropeptide signaling. Data indicate that cAMP is the primary regulator of catabolic, anabolic, and transport processes, which ultimately support the capacity for ecdysteroid production by the molting gland. While cAMP also regulates facultative ecdysteroidogenesis to some extent, cGMP appears to be the primary signaling molecule responsible for acute regulation of ecdysteroid synthesis and secretion. Little is known about the signaling mechanisms involved in the alteration of responsiveness to neuropeptides over the molt cycle. During premolt, the Y-organ becomes progressively less responsive to MIH. In the hypothetical model of MIH signaling presented, changes in MIH pulses are translated through cAMP transients to cue the alterations in gene expression responsible for decreased responsiveness. Gene expression is altered directly via cAMP-dependent kinases and indirectly though cGMP-dependent kinases and nitric oxide. Supported by NSF IBN-0342982 and ISO-075224)