I study the molecular processes that allow cells to replicate areas of the genome that contain DNA damage.  These processes, referred to as DNA damage tolerance mechanisms, are required for cell proliferation and generate many of the mutations that contribute to genetic variation and cancer development. 

Our approach is to treat cells as a physicist might, introducing defined perturbations and accurately measuring system behavior using live-cell imaging and other quantitative methods. The goal of the research is to first understand the basic logic of the DNA damage response, and then develop predictive quantitative models of the molecular processes that govern the dynamics of DNA replication, DNA damage tolerance, and cell cycle progression.