- Postdoctoral Fellow, Children's Hospital/Harvard Medical School, Boston, Mass.
- Ph.D., Cell & Developmental Biology, Stony Brook University, Stony Brook, N.Y.
- M.S., Genetics, University of Connecticut, Storrs, Conn.
- B.S., Biolochemistry, Boston College, Newton, Mass.
- Associate Scientist, Sanford Research/USD
- Assistant Professor, USDSSM
Research in the Lee Lab is devoted to understanding cilia biology through identification and characterization of genes required for motile cilia function in mouse models of the pediatric disorder primary ciliary dyskinesia (PCD). PCD affects approximately 1 in 16,000 newborn children worldwide and is commonly characterized by chronic sinusitis (sinus infection), male infertility, situs inversus (a reversal of left-right asymmetry), and hydrocephalus (water on the brain).
This syndrome results from dysfunction of motile cilia and flagella. Motile cilia extend from the surface of respiratory epithelial cells, ependymal cells lining the ventricular surface of the brain, and nodal cells in the early embryo, and they are required for clearance of fluid and particles over the surface of the cells. In addition, the structurally related sperm flagella are required for sperm motility. While the importance of cilia and flagella in human health is clear, the molecular mechanisms underlying cilia function are still under investigation. In the lab, we use traditional and emerging genetic approaches to identify genes required for cilia function in mouse models of PCD. We are also using cutting-edge biochemical and cell biological techniques to identify the molecular mechanisms regulating motile cilia function. Understanding the underlying genetic and molecular mechanisms will ultimately lead to improved methods of diagnosis and treatment of PCD and its associated disorders.