Protein degradation mechanisms modulate abscisic acid signaling and responses during abiotic stress.

Abiotic stresses such as salinity, drought, high temperature or freezing can be perceived, in part, as a transient or permanent hyperosmotic stress by the plant cell. As sessile organisms, the detrimental effects of these environmental insults limit plants productivity but also their geographical distribution. Sensing and signaling events that detect the hyperosmotic (or simply osmotic) stress involve the cellular increase of active abscisic acid (ABA). The stress phytohormone ABA regulates fundamental growth and developmental processes in the plant by marshalling metabolic and gene-expression reprogramming. Among the ABA-responsive genes, some are strictly ABA-dependent in that their expression is almost undetectable in absence of elevated levels of cellular ABA, thus their physiological role may be required only transiently. In addition, ABA-dependent modulation of some of the signaling effectors can be irreversible. In this review, without any pretention to being exhaustive, we use specific examples to illustrate how mechanistically conserved eukaryotic cell proteolytic pathways affect ABA-dependent signaling. We describe how defined proteolysis mechanisms in the plant cell, including Regulated Intramembrane Proteolysis (RIP), the Ubiquitin 26S Proteasomal System (UPS), the endocytic and autophagy pathways, contribute to regulate the spatiotemporal level and activity of PP2Cs (protein phosphatases 2C), and how an intriguing ABA-induced protein, the plant Translocator protein (TSPO), is targeted for degradation. Degradation of regulatory or effector molecules modulates or desensitizes ABA-dependent signaling and reestablishes cellular homeostasis.