Expression of molt inhibiting hormone, mTOR, and NO signaling genes in the land crab, Gecarcinus lateralis


Meeting Abstract

P1-145  Sunday, Jan. 4 15:30  Expression of molt inhibiting hormone, mTOR, and NO signaling genes in the land crab, Gecarcinus lateralis SCHULZ, H.M.*; PITTS, N.L.; MYKLES, D.L.; Colorado State University, Fort Collins ; Colorado State University, Fort Collins; Colorado State University, Fort Collins hmschulz@rams.colostate.edu

In decapod crustaceans, molting is negatively regulated by the release of molt-inhibiting hormone (MIH) from the X-organ (XO)/sinus gland (SG) complex in the eyestalk ganglia (ESG). The mechanisms controlling MIH synthesis and release in the ESG are poorly understood. MIH expression is relatively constant over the molt cycle, suggesting that MIH is regulated posttranscriptionally. As mTOR controls protein synthesis and nitric oxide (NO) is a neuromodulator, expression of mTOR (mTOR, S6K, Rheb, and Akt) and NO (NO synthase – NOS and guanylyl cyclase – GC) signaling genes were quantified over the molt cycle using qPCR. Animals were induced to molt by multiple leg autotomy and ESG were harvested from intermolt, premolt, postmolt, and blocked animals. There were no significant changes in NOS and NO-dependent or independent (GC-II and -III) GC mRNA levels over the molt cycle. Molting also had no effect on mTOR, S6K, Rheb, and Akt mRNA levels. However, expression of all genes, except Akt and GC-III, was significantly different between blocked and molting animals, suggesting that these signaling pathways are involved with molt induction. ESG is the primary source of MIH. However, other tissues, such as brain, thoracic ganglion, and limb regenerates may also express MIH. In Carcinus maenas, MIH is expressed in brain and thoracic ganglion and MIH mRNA is detected in Uca pugilator limb regenerates. Expression of MIH will be examined in G. laterals brain, thoracic ganglion, and limb regenerates. Supported by NSF (IOS-1257732).

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