Office: Biology 210
Phone: 9704917616
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About
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.