Autophagy is a cell biological process used to recycle cytoplasmic organelles and other constituents by delivering them to the lysosome for degradation. The past decade has seen an exponential expansion of our understanding of the molecular and cellular mechanisms of autophagy. Autophagy is tied to stress responses through a number of key signaling pathways, and is orchestrated by a series of core autophagy proteins (ATG proteins) that are evolutionarily conserved. The ATG proteins and genes constitute an integrated system that controls the internal milieu of the cell to support the multiple specialized functions that free-living cells, or cells in metazoan organisms, must perform. The ATG proteins, and the degradative function of autophagy, have been studied in single-celled organisms, model metazoan organisms, and mammals. Together these studies have proven that autophagy and ATG proteins play essential roles in host defense, development, organ and metabolic homeostasis, cancer, inflammation, and neurodegeneration.
This Gordon Research Conference will focus on the most up-to-date and innovative science on the area of autophagy and ATG proteins. We will begin with analysis of the fundamental mechanisms of autophagosome biogenesis and the degradative process of autophagy. Recent advances in the regulation of autophagy and the identification of signaling mechanisms responsible for the coordinate regulation of this pathway during stress, development, and disease will be emphasized. Attention will be paid to functions of ATG proteins in cellular processes that are distinct from degradative autophagy, but that nevertheless contribute to important biological functions of cells. Our emphasis will then turn to the role of autophagy and ATG proteins in cellular stress responses, organ function, and disease. We will seek to integrate diverse perspectives on the role of autophagy and ATG proteins from the fields of genetics, cell biology, structural biology, systems biology, metabolism, host defense and inflammation, cancer, and neurodegeneration.