Meeting Abstract

P2.140  Saturday, Jan. 5  Comparing the effects of molt manipulation on mechanistic Target of Rapamycin (mTOR) in molting gland (Y-organ) of blackback land crab, Gecarcinus lateralis and green shore crab, Carcinus maenas ABUHAGR, A. M.*; CHANG, E. S.; MYKLES, D. L.; Colorado State University; 2UC Davis Bodega Marine Laboratory, Bodega Bay, California; Colorado State University aliabuhagr@gmail.com

Regulation of the molt cycle in decapod crustaceans is controlled by the X-organ/sinus gland complex in the eyestalks. The complex secretes molt-inhibiting hormone (MIH) that suppresses production of molting hormone (ecdysteroids) by molting glands (Y-organs or YOs). In most decapods molting is induced by eyestalk ablation (ESA), or autotomy of 5 or more walking legs (Multiple Leg Autotomy, MLA). However, the green shore crab C. maenus (both color morphs) is refractory to ESA and MLA. The mechanistic Target of Rapamycin (mTOR) pathway is highly conserved among all metazoans; it functions as a nutrient sensor for cellular growth and is up-regulated in mammalian cancers. cDNAs encoding mTOR components (mTOR, Rheb, Akt, and S6K) were cloned from land crab, Gecarcinus lateralis, and green crab, Carcinus maenas. The purpose of this study was to quantify and compare the effects of molt manipulation (ESA and MLA), on mTOR pathway components (mTOR, Rheb, Akt, and S6K), in G. lateralis and C. maenas by qPCR. mTOR, which controls global translation of mRNA into protein, appears to be involved in YO activation. Rapamycin, an mTOR inhibitor, is a potent inhibiter of YO edysteroidogenesis. YO activation is required for transition to the committed state, as indicated by the prolonged effect of rapamycin on ESA animals. We hypothesize that up-regulation of mTOR signaling is necessary for YO hypertrophy and increased ecdysteroidogenesis during premolt. qPCR data indicate that ESA activates mTOR signaling in the G. lateralis YO, but not in the C. maenas YO. Supported by NSF (IOS-0745224).