Plant gas exchange is regulated by guard cells that form stomatal pores.
Stomatal adjustments are crucial for plant survival; they regulate
uptake of CO2 for photosynthesis, loss of water, and entrance of air
pollutants such as ozone. We mapped ozone hypersensitivity, more open
stomata, and stomatal CO2-insensitivity phenotypes of the Arabidopsis
thaliana accession Cvi-0 to a single amino acid substitution in
MITOGEN-ACTIVATED PROTEIN (MAP) KINASE 12 (MPK12). In parallel, we
showed that stomatal CO2-insensitivity phenotypes of a mutant cis
(CO2-insensitive) were caused by a deletion of MPK12. Lack of MPK12
impaired bicarbonate-induced activation of S-type anion channels. We
demonstrated that MPK12 interacted with the protein kinase HIGH LEAF
TEMPERATURE 1 (HT1)-a central node in guard cell CO2 signaling-and that
MPK12 functions as an inhibitor of HT1. These data provide a new
function for plant MPKs as protein kinase inhibitors and suggest a
mechanism through which guard cell CO2 signaling controls plant water
management.