I hold a PhD (1990) in experimental medicine from McGill. I trained with Webster Cavenee at the Ludwig Institute for Cancer Research, and it was there that I first became interested in molecular pathways of differentiation and development as potential pathogenetic mechanisms of human disease. Specifically, what interested me most was the idea that mutations that affect the timing of individual steps in these pathways could result in aberrant development or even disease just as readily as mutations that compromise the nature of the steps themselves. That is, the timing of gene activity is just as important as the activity itself. I did a postdoc with Peter Stambrook at the University of Cincinnati, where we tried for the first time to create a model system based on the lac operon of E. coli that would make it possible for us to regulate when and for how long genes were expressed. My group here at the University of Virginia is the first to get this system to work in the laboratory mouse and to use this powerful tool successfully to control transgene expression. With the lac system in place, we can finally ask, What happens when the normal activity of a gene is misplaced in time? We can also ask, What effect does timing have on how a particular mutation is expressed in an individual? Is the phenotype more severe in an individual in which the mutation is activated during development than in an individual in which it is not activated until adulthood? And, during development, can we get cell type-specific phenotypes from the same mutation by activating it at different times? Questions such as these that are relevant to understanding fundamental disease processes can now begin to be answered within an experimental system, the mouse, that is our closest human genetic model.
Selected Publications:
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This page was last updated:
Jan. 9, 2003 
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