Abscisic Acid Inhibits Type 2C Protein Phosphatases via the PYR/PYL Family of START Proteins

TLDR

Type 2C protein phosphatases (PP2Cs) are vitally involved in abscisic acid (ABA) signaling. Pyrabactin acts through PYRABACTIN RESISTANCE 1 (PYR1), the founding member of a family of START proteins called PYR/PYLs, which are necessary for both pyrabactin and ABA signaling in vivo. The study demonstrates that pyrabactin, a selective ABA agonist, activates PYR/PYL START proteins (e.g., PYR1) to bind and inhibit PP2Cs, establishing PYR/PYLs as ABA receptors at the top of a negative regulatory pathway and showcasing the utility of chemical genetics to bypass genetic redundancy.

Abstract

Type 2C protein phosphatases (PP2Cs) are vitally involved in abscisic acid (ABA) signaling. Here, we show that a synthetic growth inhibitor called pyrabactin functions as a selective ABA agonist. Pyrabactin acts through PYRABACTIN RESISTANCE 1 (PYR1), the founding member of a family of START proteins called PYR/PYLs, which are necessary for both pyrabactin and ABA signaling in vivo. We show that ABA binds to PYR1, which in turn binds to and inhibits PP2Cs. We conclude that PYR/PYLs are ABA receptors functioning at the apex of a negative regulatory pathway that controls ABA signaling by inhibiting PP2Cs. Our results illustrate the power of the chemical genetic approach for sidestepping genetic redundancy.