Jacqueline E. Lee

Molecular, Cellular & Developmental Biology; Member of the Center for Neuroscience

Department of Molecular, Cellular & Developmental Biology, Campus Box 347
MCDB Addition A245C
University of Colorado at Boulder
Boulder, CO 80309-0347

email: Jackie.Lee@colorado.edu
Phone: 303-492-6703
FAX: 303-492-7744
Website: http://mcdb.colorado.edu/faculty/lee99.html

Dr. Lee received her B.S. in Molecular Biology from the University of Wisconsin at Madison in 1985 and Ph.D. in Genetics and Development from Columbia University in New York in 1991. After completing her postdoctoral work with Dr. Harold Weintraub at the Fred Hutchinson Cancer Research Center, Seattle, WA, she had been a faculty member in the Department of Pediatrics at the University of Colorado Health Sciences Center for two years before moving to the University of Colorado at Boulder. During her postdoctoral work, she discovered NeuroD, a trancription factor capable of converting embryonic ectoderm into fully differentiated neurons. Since then, her team has determined that NeuroD plays a critical role in differentiation and survival of pancreatic beta cells and a subset of neurons, including granule cells of the hippocampus and cerebellum as well as cochlear ganglia in the inner ear. Thus, mice lacking NeuroD are diabetic, ataxic and deaf. Currently, members of her laboratory are working to determine the molecular and cellular basis of NeuroD-null phenotypse and the signaling pathways that control NeuroD activity.

Selected Publications:

Lee, J.E., S. Hollenberg, L. Snider, D. Turner, N. Lipnick and H. Weintraub (1995). Conversion of Xenopus ectoderm into neurons by NeuroD, a new basic helix-loop-helix protein. Science 268:836-844.

Miyata, T., T. Maeda and J.E. Lee (1999). NeuroD is required for differentiation of the granule cells in the cerebellum and hippocampus. Genes & Dev. 13:1647-1652.

Kim, W.Y., Fritzsch, B., Serls, A., Bakel, L.A., Huang, E. J., Reichardt, L.F., Barth, D.S., Lee, J.E. (2001). NeuroD-null mice are deaf due to a severe loss of the inner ear sensory neurons during development. Development 128: 417-426.