PYRABACTIN RESISTANCE 1 – LIKE 8 and AKT1 INTERACTING PROTEIN PHOSPHATASE 1 are involved in ammonium transport regulation

Plants perceive high ammonium concentrations as an abiotic stress that triggers ABA (abscisic acid) signaling. ABA signaling leads to a phospho-regulatory cascade involving the PP2C phosphatase ABI1 (PROTEIN PHOSPHATASE 2C ABA INSENSITIVE 1) and kinase CIPK23 (CBL INTERACTING PROTEIN KINASE 23). ABI1 is inactivated by ABA, releasing the kinase CIPK23 to phosphorylate and inactivate AMT1 (AMMONIUM TRANSPORTER 1) transporters. To date, it was unclear whether this effective mechanism to prevent ammonium toxicity relies on various ABA sensors and general signaling or whether a specific ABA sensor is involved in this regulation. Here, we show that ammonium stress specifically induces the expression of a subset of PYL (PYRABACTIN RESISTANCE 1 - LIKE) ABA receptors, including PYL8. PYL8 is known to preferably bind and regulate the PP2C phosphatase AIP1 (AKT1 INTERACTING PROTEIN PHOSPHATASE 1). Addressing the upregulated PYLs, only a pyl8 mutant showed an increased sensitivity to high ammonium concentrations and a growth retardation in the response to high external ammonium conditions. Correspondingly, aip1 mutants showed a lower sensitivity and a delay in AMT1 reactivation. While AMT1 inactivation appears to be a general mechanism regulated by ABI1 and several PYLs, the function of AIP1 and PYL8 seems to be the regulation of AMT1 reactivation.