Research

Our lab studies mechanisms by which cell architecture controls cell function. In the past, much of our work has been focused on linking cytoskeleton dynamics to cell functions such as migration, mitosis, and molecular trafficking. We have made significant contributions to current models of the dynamic organization of the cytoskeleton in motile cells and during cell polarization, to models of the mitotic spindle, and to the organization of GTPase signaling programs that coordinate these dynamics.
The staple of our work has been the integration of live cell imaging and computer vision with molecular cell biology. We like to do things other labs do not do!
Our goal is to deploy computer science to cell biological experiments that lead to the discovery of cellular mechanisms, which escape purely experimental approaches. Inspired by questions in cell biology, our lab has brought significant innovation also to computer vision and statistical modeling.
In 2014 our lab moved from Harvard Medical School to UT Southwestern Medical Center. We seized the opportunity of a new environment to shift our research towards non-genomic mechanisms that promote the plasticity in proliferation/survival necessary for cancer cells to accommodate variable environments. Of particular current interest to the lab is the question how cell shape and cytoskeleton architecture directly control proliferation/survival signaling and metabolism. The notion that morphology by itself controls cellular signaling is underappreciated in cell biology and new in the context of cancer. Our research in this arena is empowered by our close collaborations with Reto Fiolka, Kevin Dean, and their teams, who develop microscopy approaches to visualize cell behavior, so that we can apply frameworks of causal inference to establish the hierarchy between morphology and signaling.

Non-genetic mechanisms controlling cancer cell function.

Stochasticity and feedbacks, as well as environmental inputs, often disconnect the genomic state of a cancer cell from the disease-driving functions of enhanced proliferation, survival, and –perhaps – migration. Our lab thus develops analytical and experimental technologies that capture the functional states of cancer cells and their regulation by integrated circuits of cytoskeleton architecture, signaling, and metabolism in variable environmental context. Currently, we are particularly interested in the roles cell morphology plays as a regulator of cell signaling and metabolism.