• 1984-1999, Assistant and Associate Professor, Cellular Biology and Anatomy, Medical College of Wisconsin
• 1999-present, Associate Professor, Pathology and Anatomy, EVMS

Teaching

• Medical Histology

Biomedical Sciences Graduate Program Track

• Cell Biology and Molecular Pathogenesis

Basic Science Research Focus Group

• Neuroscience

Education

• B.S., Biochemistry, University of Wisconsin - Madison
• Ph.D., Biology, Johns Hopkins University

Research Interests

Molecular basis of synapse formation

My primary research interest is to understand molecular signals that cause formation and differentiation of synapses during embryonic development. This work is focused on the embryonic neuromuscular junction (NMJ). Currently we are using the frog embryo Xenopus laevis to study development of nerve-muscle synapses. Much of my past work has focused on agrin, a protein released from motor nerve terminals that directs the formation and organization of the postsynaptic apparatus of the skeletal muscle cell at the NMJ. Agrin works through several proteins in muscle cells, including its receptor, muscle-specific kinase, and alpha-dystroglycan. We are using RNA and DNA injection and making transgenic embryos to overexpress and misexpress these proteins during synapse formation, in order to better understand their role in development of the embryonic synapse.

1.5 day old Xenopus embryo expressing green fluorescent protein encoded by a DNA vector

Another interest is identifying and characterizing signaling molecules from muscle cells that direct the organization of motor nerve terminals. This new direction may involve DNA microarray and proteomic approaches to identifying these molecules.

Our work relates to neuromuscular diseases, especially Duchenne muscular dystrophy, in which the protein dystrophin is missing or mutated. The agrin-binding protein dystroglycan is part of a dystrophin-associated complex in the muscle cell membrane. Dystrophin and dystroglycan may also be involved in organizing synapses in the brain, since these proteins are concentrated at these synapses, and many muscular dystrophy patients suffer from learning disabilities.

Selected Publications

• Godfrey, E.W., Roe, J., and Heathcote, R.D. Overexpression of agrin isoforms alters the distribution of synaptic acetylcholine receptors during development of the neuromuscular junction. Devel. Biol. 205:22-32, 1999.
   
• Godfrey, E.W., Roe, J, and Heathcote, RD Agrin fragments differentially induce ectopic aggregation of acetylcholine receptors in myotomal muscles of Xenopus embryos. J. Neurobiol. 44:436-445, 2000.
   
• Heathcote, RD, Ekman, J., Campbell, K.P., and Godfrey, E.W. Dystroglycan overexpression inhibits acetylcholine receptor aggregation at embryonic Xenopus neuromuscular synapses. Devel. Biol. 227: 595-605, 2000.

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