Colorado State University

Our research concerns the regulation of molting and skeletal muscle plasticity in crabs and lobsters. Specific areas are signaling mechanisms in the molting gland and proteolytic mechanisms mediating molt-induced claw muscle atrophy. Quantitative methods are used to measure transcriptional and post-transcriptional regulation of signal transduction of molt-inhibiting hormone (MIH), a neuropeptide that inhibits ecdysteroid synthesis in the molting gland and myostatin, a TGFß superfamily member that induces skeletal muscle atrophy. Signaling mechanisms in crustacean molting gland. Growth in crustaceans requires the periodic shedding of the shell, a process called molting, which is controlled by a neurosecretory center in the eyestalks. The complex secretes MIH that inhibits production of the molting hormone ecdysone, an ecdysteroid secreted by a pair of molting glands (Y-organs or YOs) located in the body. Thus molting is triggered by a reduction in MIH in the blood, which stimulates the YOs to synthesize and secrete ecdysone. Binding of MIH to a membrane receptor results in a cyclic nucleotide-dependent inhibition of mechanistic Target of Rapamycin (mTOR), a highly conserved protein kinase that controls protein synthesis. The YO transitions to a committed state during premolt that requires TGFß signaling. Transcriptomics and proteomics are being used to understand the genetic mechanisms of YO transitions during the molt cycle.