Donald Mykles Professor; Director University Honors Program

Office: Academic Village Honors Progra B102

Phone: (970) 491-5679

Website: https://rydberg.biology.colostate.edu/mykleslab

Education

  • Ph.D., University of California, Berkeley

About

Fall 2012 Newsletter Spring 2012 Newsletter Fall 2011 Newsletter Spring 2011 Newsletter Fall 2010 Newsletter Spring 2010 Newsletter Fall 2009 Newsletter Spring 2009 Newsletter Fall 2008 Newsletter Spring 2008 Newsletter 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. Regulation of muscle atrophy by myostatin. In mammals myostatin (Mstn) is a negative regulator skeletal muscle growth. We hav identified Mstn orthologs in crabs and lobsters. As these genes are preferentially expressed in skeletal muscle, they may have similar functions in invertebrates. We are examining the role of Mstn in controlling molt-induced claw muscle atrophy, in which the claw muscle mass is reduced as much as 78% before molting. The reduced mass facilitates withdrawal of the large claws through the narrow joints that connect the appendage to the body. Binding of Mstn to a membrane receptor results in phosphorylation of Smad proteins. Smads are transcription factors that translocate to the nucleus and alter gene expression. cDNAs encoding land crab Smads have been obtained. Quantitative RT-PCR and proteomic analysis are used to measure Smad mRNA and protein levels, respectively. Image analysis are used to quantify Smads in the nucleus and cytoplasm in response to Mstn.

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