SEC16A/MAG5-mediated ER export shapes ABA receptor homeostasis

Loss of SEC16A/MAG5 disrupts early secretory trafficking of the ER–Golgi pool of PYR1 and PYL4, causing receptor accumulation and enhanced ABA signalling.

• Why it matters: ABA receptor activity depends on regulated turnover, but how receptor homeostasis is set up in the early secretory pathway was unknown.
• What they did: Using cell biological and biochemical assays, the study identified a constitutive ER/Golgi-associated pool of PYR1 and PYL4 and tested trafficking and signalling after MAG5 disruption via genetic, pharmacological, and imaging approaches.
• The result: MAG5 is required for proper trafficking to late endosomal compartments; its loss increases intracellular receptor accumulation and enhances ABA signalling without changing endogenous ABA levels.

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