SEC16A/MAG5-mediated ER export shapes ABA receptor homeostasis

The phytohormone abscisic acid (ABA) controls plant adaptation to environmental stress through PYR/PYL/RCAR receptors. Regulated receptor turnover through ubiquitination and endosomal trafficking, including ESCRT-dependent vacuolar degradation, is a major mechanism controlling ABA signalling. However, whether ABA receptor homeostasis is established during the early secretory pathway remains unknown. Using complementary cell biological and biochemical approaches, we define a constitutive early secretory pool of the ABA receptors PYR1 and PYL4 associated with the endoplasmic reticulum (ER) and the Golgi apparatus (GA). Genetic, cell biological and pharmacological analyses reveal that the COPII scaffold protein SEC16A (also known as MAG5) is required for the proper trafficking and homeostasis of this receptor pool. Loss of MAG5 causes intracellular receptor accumulation, impaired trafficking towards late endosomal compartments and enhanced ABA signalling without affecting endogenous ABA accumulation. Together, our findings establish the early secretory pathway as an integral component of the ABA signalling network and demonstrate that MAG5-mediated ER export shapes ABA receptor homeostasis by coordinating receptor trafficking throughout the endomembrane system, revealing the ER as a key regulatory compartment for ABA receptor homeostasis.