Meeting Abstract

P2.138  Saturday, Jan. 5  mTOR-dependent protein synthesis is required for ecdysteroid synthesis in the crustacean molting gland HEAD, T. B.*; MUDRON, M. R.; CHANG, S. A.; CHANG, E. S. ; MYKLES, D. L. ; Colorado State University; Colorado State University; UC Davis Bodega Marine Laboratory; UC Davis Bodega Marine Laboratory; Colorado State University talhead@rams.colostate.edu

Molting in crustaceans is regulated by two endocrine organs: the X-organ (XO)/sinus gland complex in the eyestalks and a pair Y-organs (YOs) located in the thoracic region. The XO produces molt-inhibiting hormone (MIH), which inhibits synthesis of molting hormones (ecdysteroids) by the YO. Our model of the MIH signaling pathway in the YO involves a cAMP/calcium-dependent “triggering” phase and a NO/cGMP-dependent “summation” phase. A potential downstream target is mechanistic Target of Rapamycin (mTOR), a protein kinase that regulates translation of mRNA into protein. This ongoing study determines the effects of recombinant MIH and reagents that target components of MIH and mTOR signaling on YO ecdysteroidogenesis. YOs from the green shore crab, Carcinus maenas, were cultured in the presence or absence of a compound and ecdysteroids secreted to the medium were quantified by ELISA. cPTIO (NO scavenger) (p = 0.022) and ODQ (NO-dependent guanylyl cyclase inhibitor) (p = 0.039) increased ecdysteroid secretion. Cyclohexamide (RNA translation inhibitor) (p = 0.0003) inhibited ecdysteroid secretion. Actinomycin D (mRNA synthesis inhibitor) had no significant effect. Previous work showed that the mTOR antagonist rapamycin is a potent inhibitor of YO ecdysteroidogenesis. The data suggest that MIH signaling inhibits mTOR and that translational control by mTOR is necessary for maximal ecdysteroid synthesis by the YO. Supported by NSF (IOS-0745224).