Autophagy is a conserved catabolic process that initially involves the bulk or the selective engulfment of cytosolic components into double-membrane vesicles and successively the transport of the sequestered cargo material into the lysosome/vacuole for degradation. This pathway allows counteracting internal and external stresses, including changes in the nutrient availability, that alter the cell metabolic equilibrium. Consequently, the regulation of autophagy is crucial for maintaining important cellular functions under various conditions and ultimately it is essential for survival. Yeast Saccharomyces cerevisiae has been successfully employed as a model system to study autophagy. For instance, it has allowed the isolation of the factors specifically involved in autophagy, the Atg proteins, and the characterization of some of their molecular roles. In addition, this organism also possesses all the principal signaling cascades that modulate the cell metabolism in response to nutrient availability in higher eukaryotes, including the TOR and the PKA pathways. Therefore, yeast is an ideal system to study the regulation of autophagy by these signaling pathways. Here, we review the current state of our knowledge about the molecular events leading to the induction or inhibition of autophagy in yeast with special emphasis on the regulation of the function of Atg proteins.