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Developmental Biology - Research Overview and Interests


The Section of Developmental Biology originated in 2004 through support of Children’s Hospital Colorado Research Institute and was significantly expanded in 2008 through a gift from the Gates Frontier Fund. Grants from both public (NIH) and private foundations (Howard Hughes Medical Institute, Juvenile Diabetes Research Foundation, American Asthma Foundation, National Multiple Sclerosis Society) have helped to support the research programs of the faculty within the Section.

Research into birth defects and childhood diseases utilizes animal models that have been created in the Section to elucidate the molecular and cellular processes that regulate normal development. Sophisticated microscopy equipment that has been obtained by the Section provides new insight by allowing the visualization of dynamic developmental processes. Collaborations with other groups at Children's Colorado and the School of Medicine, as well as groups around the nation, have enhanced our ability to pinpoint mutant genes, to generate new animal models, to identify the complex group of molecules that are made in specific cells, and to screen for chemicals of potential therapeutic importance.

Dr. Bruce Appel’s long-term interests are to identify genes that are targets for therapies to treat developmental, degenerative, and cancerous diseases of the nervous system. He uses zebrafish as a model system to understand the mechanisms that produce and maintain neural precursors and that direct the formation of distinct neurons and glia.

Dr. Lee Niswander’s work focuses on closure of the neural tube and the development of the limb and lung. Her research in the mouse embryo has provided novel insights into the molecular mechanisms that control these developmental processes. The lab has created methods to follow these developmental events in real time and has combined dynamic imaging with genetic models to elucidate how these genes act to regulate cell behaviors. Her lab’s research also explores gene-environment interactions that alter the risk of neural tube defects, in particular the molecular mechanisms underlying the responsiveness to folic acid supplementation.