Opposing modulation of QUAC1/ALMT12 by S-type channel inhibition and R-type channel activation during elevated-CO2 and ABA-induced stomatal movement

Atmospheric CO₂ concentrations, now 50% higher than pre-industrial levels, induce plant stomatal closure. The slow (S)-type anion channels in guard cells are activated by elevated CO₂/bicarbonate and promote that process. However, the response of the rapid (R)-type anion channels to CO₂/bicarbonate remains unclear. Here, we show that bicarbonate fails to activate the R-type anion channel QUAC1 (ALMT12) in either Xenopus oocytes or guard cell protoplasts, which indicates that the two channel types are differentially in response to CO₂/bicarbonate. Furthermore, we demonstrate that QUAC1/ALMT12 negatively regulates CO₂/bicarbonate-induced stomatal closure, achieved through its inhibition of SLAC1. As such, ALMT12 has opposite functional consequences in ABA vs CO₂ pathways due to differential upstream activation.