Our research focuses on the lysosome-mediated cellular degradation pathways. We investigate how apoptotic cells are degraded by the lysosome and how lysosome dynamics and functions are regulated using C. elegans as a model system.
Lysosomes degrade macromolecules and recycle catabolites to maintain cell homeostasis. They serve as a signal hub to detect environmental changes and coordinate cellular responses. Lysosomes are extremely important for animal physiology and impairment of lysosome function contributes to many diseases including lysosomal storage diseases, neurodegenerative disorders, and cancer. Surprisingly, we understand very little about how lysosome functions are achieved under physiological conditions and how lysosome dysfunction leads to pathogenesis of human diseases. By developing and employing C. elegans as a multicellular genetic model, we aim to systematically dissect regulatory mechanisms that control lysosome hemostasis and reveal the physiological significance.
Phagocytic removal of apoptotic cells is an integral part of the cell death program and important event in tissue remodeling, suppression of inflammation and regulation of immune response. Using C. elegans as a model and employing combinatory approaches of genetics, cell biology and biochemistry, we have identified new genes and have dissected regulatory mechanisms that control various aspects of apoptotic cell removal including recognition, internalization and lysosomal degradation of cell corpses.