Meeting Abstract
60.5 Tuesday, Jan. 6 Myostatin Signaling and the Regulation of a Molt-Induced Atrophy in Crustacean Claw Muscle COVI, J.A.; BADER, B.A.; WASMUNDT, N.M.; CHANG, E.S.; MYKLES, D.L.*; Colorado State University; Colorado State University; Colorado State University; UC Davis Bodega Marine Lab; Colorado State University don@lamar.colostate.edu
Molt-induced claw muscle atrophy is under the control of steroid molting hormones (ecdysteroids). The reduction of as much as 78% of the muscle mass, which facilitates withdrawal of the claws at molt (ecdysis), is achieved by the degradation of myofibrillar proteins by calpains. Only the claw muscles are responsive to the atrophy-inducing signal. Thoracic muscle, which does not respond to ecdysteroid, serves as an internal control. Moreover, there is no transformation of fiber phenotype or satellite cells. Thus, crustaceans provide an ideal model system in which the molecular mechanisms regulating protein turnover can be studied apart from those regulating fiber phenotype transformation or satellite cell proliferation. The central hypothesis is that the action of ecdysteroids is mediated by myostatin (Mstn)/Smad signaling. cDNAs encoding Mstn and Smad transcription factors were cloned from three decapod species (land crab, green crab, and lobster). Isoforms differing in the length and/or sequence of the Mstn propeptide appear to be generated by alternative splicing. The effects of two methods of molt induction on Mstn expression were determined in the land crab, Gecarcinus lateralis. Acute elevation of hemolymph ecdysteroids by eyestalk ablation (ESA) increases Mstn mRNA in claw muscle but not thoracic muscle. In contrast, molting induced by multiple limb autotomy decreases Mstn mRNA in both claw and thoracic muscles during premolt. These data suggest that Mstn expression is regulated by ecdysteroid hormone, but nature of the tissue response depends on the method used to induce molting. This indicates that ESA cannot be used mimic the transition from intermolt to premolt stages in intact animals. Supported by NSF (IOS-0618203).
