Autophagy is a ubiquitous process used widely across plant cells to degrade cellular material and is an important regulator of plant growth and various environmental stress responses in plants. The initiation and dynamics of autophagy in plant cells are precisely controlled according to the developmental stage of the plant and changes in the environment, which are transduced into intracellular signaling pathways. These signaling pathways often regulate autophagy by mediating TOR (Target of Rapamycin) kinase activity, an important regulator of autophagy initiation; however, some also act via TOR-independent pathways. Under nutrient starvation, TOR activity is suppressed through glucose or ROS (reactive oxygen species) signaling, thereby promoting the initiation of autophagy. Under stresses, autophagy can be regulated by the regulatory networks connecting stresses, ROS and plant hormones, and in turn, autophagy regulates ROS levels and hormone signaling. This review focuses on the latest research progress in the mechanism of different external signals regulating autophagy.

All eukaryotes rely on the ubiquitin-proteasome system (UPS) and autophagy to control the abundance of key regulatory proteins and maintain a healthy intracellular environment. In the UPS, damaged or superfluous proteins are ubiquitinated and degraded in the proteasome, mediated by three types of ubiquitin enzymes: E1s (ubiquitin activating enzymes), E2s (ubiquitin conjugating enzymes), and E3s (ubiquitin protein ligases). Conversely, in autophagy, a vesicular autophagosome is formed that transfers damaged proteins and organelles to the vacuole, mediated by a series of ATGs (autophagy related genes). Despite the use of two completely different componential systems, the UPS and autophagy are closely interconnected and mutually regulated. During autophagy, ATG8 proteins, which are autophagosome markers, decorate the autophagosome membrane similarly to ubiquitination of damaged proteins. Ubiquitin is also involved in many selective autophagy processes and is thus a common factor of the UPS and autophagy. Additionally, the components of the UPS, such as the 26S proteasome, can be degraded via autophagy, and conversely, ATGs can be degraded by the UPS, indicating cross regulation between the two pathways. The UPS and autophagy cooperate and jointly regulate homeostasis of cellular components during plant development and stress response.