Tumor Supression, Cell Death and Mobile Genetic Elements
My lab applies high throughput genetic approaches to explore two biomedical themes. One organizing theme explores the p53 regulatory network, which is deranged in most human cancers. Despite extensive characterization, precisely how p53 acts to suppress tumors remains poorly understood. We built innovative tools to interrogate p53 function in Drosophila, zebrafish and mouse models and, using these, we discovered that p53 tonically acts to supress transposons. Current projects are directed toward understanding how p53 functions to restrain mobile elements and tests the clinical utility of this 'transposopathy' model. A second and related research program examines gene-directed programs that specify programmed and unprogrammed cell death.