Denise Montell (Johns Hopkins University)
MolBio Seminar Series
Denise Montell earned her B.A. degree from the University of California, San Diego and her PhD in Neurosciences from Stanford University, where she worked on axon pathfinding with Corey Goodman. She went on to do postdoctoral work with Dr. Allan Spradling at the Carnegie Institution where she initiated studies of collective cell migration. After two years she advance to an independent "Staff Associate" position at the Carnegie and after two more years joined the faculty of the Department of Biological Chemistry at the Johns Hopkins School of Medicine. She rose to the rank of Full Professor in 2002, directed the Graduate Program in Biological Chemistry for more than 10 years, and was the founder and founding director of the interdepartmental Center for Cell Dynamics. After more than 20 years at JHU, Dr. Montell recently returned to California as the Duggan Professor of Molecular, Cellular and Developmental Biology at the University of California, Santa Barbara. In addition to her research, Dr. Montell serves on scientific advisory councils for both NIGMS and the American Cancer Society.
Life, Death and Resurrection at the Cellular Level
The ultimate goal of tissue engineering and regenerative medicine is to build functional artificial tissues. In order to achieve this, it is necessary to understand not only how each cell type is specified but also how cells decide to live or die and how they self-assemble into functional three-dimensional architectures. One approach is to decipher, and ultimately to harness, the mechanisms governing normal development. The Drosophila ovary serves as a powerful model for general aspects of organogenesis in including stem cell biology, cell fate diversification,
cell motility, morphogenesis, and the influence of physiological conditions on development. In this seminar, several questions will be discussed. What are the mechanisms that control the migrations of interconnected groups of cells, and how do these mechanisms compare to those controlling the movements of individual cells? A second question is how cells decide whether to live or die. Recent surprising studies reveal that dying cells can reverse the apoptotic process, survive and proliferate, even after sustaining DNA damage. This process has been named anastasis. While most cells repair their damaged DNA, residual genetic alterations persist in some cells and can result in oncogenic transformation. Although proliferation of transformed cells is a negative consequence, anastasis may serve useful purposes as well. For example, such a cell survival mechanism could serve to salvage postmitotic cells, which are difficult to replace, and thereby limit permanent tissue damage due to transient stresses. The DNA mutations that persist following anastasis represent a form of stress-induced mutagenesis, increasing genetic and phenotypic diversity in response to environmental or physiological stresses that initiate apoptosis. Negative side effects of this otherwise beneficial process may include carcinogenesis and evolution of drug resistance following chemotherapy.
Free and open to the university community and the public