Mounting evidence suggests that acetylation plays an important role in various biological processes including transcriptional regulation, DNA damage repair, cell cycle progression, aging, and glycolysis. It is increasingly recognized that acetylation also regulates autophagy; for example, increasing the cellular acetylation level by treating cells with histone deacetylase (HDAC) inhibitors such as TSA can promote autophagy, and knockdown of the histone acetyltransferase KAT2B/p300 induces autophagy in nutrient-rich conditions. Our goal is to dissect the molecular mechanisms underlying the seemingly complicated role of acetylation in autophagy. We used Saccharomyces cerevisiae as a model organism because it can be genetically manipulated in a relatively easy and reliable way, allowing us to test the function of acetylases, deacetylases and acetylation sites on autophagy regulation in a "clean" system.