The Alberts Laboratory studies the architecture of individual cells as they move, grow, divide, and reprogram during development, neoplasia, and in responses to injury, infection, and age. We seek to understand how cell structure defects contribute to disease acquisition and progression. The goal is to use what we learn to devise ways to repair, reinforce, or remodel cell structure for therapeutic benefit.
The lab places a special emphasis on the genetics, and the molecular and cell biology of a family of cytoskeletal assembly proteins called the Diaphanous-related formins. Named after the insect founder gene Diaphanous and a gene once thought to be a gene mutation accounting for limb deformities, we now know that formins’ conserved role in biology is to assemble microfilament and microtubule structures into a cytoskeleton that physically supports and organizes cell function.
Our studies have led to the discovery of mechanisms governing formin activity and the characterization of essential roles for the Diaphanous family in cell adhesion, migration, division, and new gene expression processes required for tumor suppression and immunity. Formin activation also induces gene expression for cell structure components via the transcription factor SRF. SRF is responsible for coordinating demands for new expression of cell structure genes along with genes promoting cellular regeneration.
Mutations and epigenetic changes affecting Diaphanous family expression and function in people have been associated with inherited deafness syndromes, autism spectrum disorders, and severe developmental delay as well as cancer. In addition to our cancer research, these discoveries have led us to pursue research in areas devoted to understanding how formins contribute to neuron infrastructure assembly and maintenance—an area of long-standing interest.