Molt-Inhibiting Hormone Signaling in the Crustacean Molting Gland Nitric Oxide and Cyclic Nucleotides


Meeting Abstract

P1.104  Jan. 4  Molt-Inhibiting Hormone Signaling in the Crustacean Molting Gland: Nitric Oxide and Cyclic Nucleotides GOMEZ, A.M.*; LEE, K.J.; COVI, J.A.; CHANG, S.A.; CHANG, E.S.; MYKLES, D.L.; Colorado State University; Colorado State University; Colorado State University; UC Davis Bodega Marine Lab; UC Davis Bodega Marine Lab; Colorado State University amg543@med.nyu.edu

Crustacean growth is regulated by ecdysteroids, which are produced in the molting glands or Y-organs (YO) located in the cephalothorax. Synthesis of ecdysteroids is suppressed by molt-inhibiting hormone (MIH), a neuropeptide produced in the eyestalk ganglia (EG). Binding of MIH to its receptor initiates a signal transduction cascade mediated by cyclic nucleotide second messengers (cGMP and/or cAMP). As YOs express nitric oxide synthase (NOS) and NO-sensitive guanylyl cyclase (GC), we used an in vitro YO assay to investigate the roles these enzymes in MIH signaling. Blackback land crabs, Gecarcinus lateralis, and European green crabs, Carcinus maenas, were eyestalk-ablated to activate the YOs; after 2 days the YOs were cultured in crab saline to measure secretion of ecdysteroid into the medium by radioimmunoassay. 8-Bromo-cGMP significantly reduced ecdysteroid secretion, while the effects of 8-Bromo-cAMP were more variable. Recombinant MIH (rMIH), EG extract, or reagents that stimulate NOS (SNAP, SE 175) or GC (YC-1) inhibited secretion. These results indicate that NO or cGMP can mimic the action of MIH on the YO. We will determine the effects of NOS and GC antagonists on rMIH suppression of ecdysteroidogenesis. Supported by NSF (IBN-0342982), Colorado Association for Minority Participation (CO-AMP), and scholarship to AMG from the Arnold and Mabel Beckman Foundation.

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