Mathematics Colloquia and Seminars
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Computational Models of Cell Mechanobiology, from Focal Adhesions to Nuclear PoresMathematical Biology
|Speaker: ||Mohammad R. K. Mofrad, UC Berkeley|
|Location: ||2112 MSB|
|Start time: ||Mon, Mar 4 2013, 3:10PM|
Cells sense mechanical signals and actively respond by altering their phenotype. Cellular mechanotransduction is mediated by a combination of biochemical and biophysical mechanisms via mechanically induced changes in the structure and function of specific molecules. These mechanosensing molecules can function to initiate key biological processes, e.g. formation of the focal adhesion machinery at the interface of cell’s interaction with the extracellular matrix. Another example of potential molecular machines likely taking part in regulation of mechanotransduction is the nuclear pore complex that controls the nucleocytoplasmic traffic, regulating gene expression and protein synthesis. In this talk, I will present some of our recent efforts aimed at better understanding of the molecular players in cellular mechanotransduction, focused on two particular molecular machineries, namely the focal adhesions and the nuclear pores. A series of molecular dynamics investigations will be presented to explore the potential mechanosensing and mechanotransduction functions of key molecules involved in focal adhesion formation. Using state-of-the-art molecular dynamics modeling and simulation techniques, the molecular mechanics of these proteins, their force-induced activation, and changes in their molecular conformation and binding partnership will be discussed. Finally, I will present our recent models to explore the exquisite function of the nuclear pores and the relationship between biochemical factors and mechanical behavior of cargo being transported across the nuclear pore.