Research

We use the nematode C. elegans as a model system for studying evolutionarily conserved signal transduction pathways that are dysregulated in human disease, with the eventual goal of generating hypotheses that can be tested in mouse models of human disease. Currently, our major focus is an insulin/insulin-like growth factor-1 pathway that regulates development, metabolism, and lifespan in C. elegans. We anticipate that our studies will be relevant to the pathogenesis of Type 2 diabetes and cancer.

C. elegans was first established as a model organism for studying development in the 1960s. Its short generation time, ease of propagation, and invariant cell lineage have made it a popular system for studying a wide variety of biological processes. In the 1980s, seminal work done in the laboratory of Nobel Laureate H. Robert Horvitz at MIT identified and characterized genes involved in programmed cell death in C. elegans. Recent research underscores the relevance of this system to human cancer pathogenesis. Comparative genome analysis, along with work from many C. elegans laboratories, has revealed the structural and functional conservation of myriad signal transduction pathways and molecules that are mutated in human disease. The elucidation of mechanisms of signal transduction in C. elegans may lead to a better understanding of human disease pathogenesis as well as the development of novel drug treatments.