Abstract: Stomata are pores at the leaf surface that facilitate CO₂ entry for photosynthesis while controlling transpirational water loss. Stomatal movements are governed by reversible changes in turgor and cell volume, driven by the transport of osmotic solute across the membrane of guard cells surrounding the pore. Membrane transport depends on the activities of transporters and ion channels present at the membrane and also on their abundance, determined by vesicle traffic. Although much is known about how pumps and ion channels in the membrane are regulated, this is not the case for vesicle trafficking and certainly not in relation to CO₂. Here, we report on experiments following the traffic of the K⁺ channel KAT1 that is important for K⁺ uptake during stomatal opening. We found that elevated CO₂ triggers changes in channel mobility within the plane of the plasma membrane and its internalization therefrom. CO₂- sensitive KAT1 traffic depends on SYP121, a vesicle-trafficking (SNARE) protein previously associated with water stress and abscisic acid (ABA) that also binds the K⁺ channel to promote its activation. The CO₂-sensitive pathway parallels vesicle traffic evoked by ABA, but it also shows important differences, with KAT1–SYP121 binding sensitive to CO₂. We show that stomatal response to changes in CO₂ levels is slowed in the syp121 null mutant, affecting shoot growth and whole-plant water-use efficiency. Thus, we uncover a new target for CO₂ regulation in vesicle traffic and a novel perspective on plant responses to climate change.

Key words: CO₂-sensing, K⁺ channel, membrane traffic, SNARE, stomata, transport