Respiration in leaves and the continued elevation in the atmospheric CO₂ concentration cause CO₂ -mediated reduction in stomatal pore apertures. Several mutants have been isolated for which stomatal responses to both abscisic acid (ABA) and CO₂ are simultaneously defective. However, there are only few mutations that impair the stomatal response to elevated CO₂ , but not to ABA. Such mutants are invaluable in unraveling the molecular mechanisms of early CO₂ signal transduction in guard cells. Recently, mutations in the mitogen-activated protein (MAP) kinase, MPK12, have been shown to partially impair CO₂ -induced stomatal closure. Here, we show that mpk12 plants, in which MPK4 is stably silenced specifically in guard cells (mpk12 mpk4GC homozygous double-mutants), completely lack CO₂ -induced stomatal responses and have impaired activation of guard cell S-type anion channels in response to elevated CO₂ /bicarbonate. However, ABA-induced stomatal closure, S-type anion channel activation and ABA-induced marker gene expression remain intact in the mpk12 mpk4GC double-mutants. These findings suggest that MPK12 and MPK4 act very early in CO₂ signaling, upstream of, or parallel to the convergence of CO₂ and ABA signal transduction. The activities of MPK4 and MPK12 protein kinases were not directly modulated by CO₂ /bicarbonate in vitro, suggesting that they are not direct CO₂ /bicarbonate sensors. Further data indicate that MPK4 and MPK12 have distinguishable roles in Arabidopsis and that the previously suggested role of RHC1 in stomatal CO₂ signaling is minor, whereas MPK4 and MPK12 act as key components of early stomatal CO₂ signal transduction.

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