This is an NIH-funded postdoctoral research position. The long-term goal of this research project is to understand how cilia function. Cilia and extracellular vesicles (EVs) are signaling organelles that play important roles in human health and disease. We recently showed that C. elegans ciliated sensory neurons release bioactive, polycystin-containing EVs. In humans, mutations in the polycystin-encoding PKD1 and PKD2 genes cause autosomal dominant polycystic kidney disease (ADPKD). In C. elegans and mammals, the polycystins act in the same genetic pathway, act in a sensory capacity, localize to cilia, and are contained in secreted EVs, indicating ancient functions. EV shedding from ciliated cells is an evolutionarily conserved phenomenon, yet remarkably little is known about the relationship between the polycystins, cilia, and EVs and the fundamental biology of EVs. The primary role of this position is to design, perform, and interpret experiments to address central questions regarding the biology of cilia, EVs, and the polycystins.