Meeting Abstract

42.4  Saturday, Jan. 5  Comparative assessment of Smad expression in two models of muscle atrophy for the blackback land crab, Gecarcinus lateralis COVI, J.A.*; BADER, B.D.; CHANG, E.S.; MYKLES, D.L.; Univ. of North Carolina at Wilmington; Colorado State Univ.; Bodega Marine Laboratory; Colorado State Univ.

In decapod crustaceans, reversible atrophy of claw muscle is imperative for successful withdrawal of the claw at ecdysis. The execution of this regulated atrophy is under the control of molting hormones termed ecdysteroids. By contrast, thoracic musculature atrophies in response to unweighting, but not elevated ecdysteroids. Published data for Gecarcinus lateralis support a role for a myostatin-like factor in mediating both atrophy induced by unweighting and atrophy regulated by ecdysteroids, albeit by what appear to be different regulatory strategies. Myostatin is a member of the TGF-β superfamily well known for its role as a negative regulator of muscle mass in mammals. Transduction of the myostatin signal between its membrane-bound receptor and the nucleus is dependent on a family of transcription factors known as Smads. Phosphorylation of R-Smad by the myostatin receptor initiates Smad activation and translocation to the nucleus. Inhibitory Smads (I-Smad) limit the duration of the myostatin signal by antagonizing the action of R-Smads. Both I-Smad and R-Smad are expressed in decapod skeletal muscle. Expression of R-Smad mRNA in both unweighted and weighted thoracic muscle did not change appreciably during a molting cycle initiated by multiple limb autotomy. However, R-Smad expression increased significantly in claw muscle during premolt, and decreased over 3.5 fold during postmolt. Expression of R-Smad during a molt cycle initiated by eyestalk ablation presented a different response; R-Smad copy number decreased during premolt in claw and thoracic muscle. This suggests that R-Smad expression in skeletal muscle is regulated, in part, by a factor produced in the eyestalks. Supported by NSF (IBN-0618203)