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Abstract Stomatal pores in land plants rapidly and reversibly open and close in response to diurnal changes in leaf carbon dioxide (CO2) concentration. Studies have suggested that CO2 is sensed by guard cells with relevant amplifying contributions from mesophyll tissue. CO2 concentration changes trigger rapid signal transduction events involving protein phosphorylation in guard cells. Moreover, molecular crosstalk and physiological interactions of the stomatal CO2 response with other environmental conditions and stimuli, including light, temperature, drought, and abscisic acid, are reviewed here. Genetic studies have revealed several key genes and provided important insights into the stomatal CO2 sensors and signal transduction mechanisms. The primary CO2/HCO3− sensor in Arabidopsis guard cells was recently identified. Quantitative trait locus (QTL) analyses have shown that early guard cell CO2 signal transduction components regulate water use efficiency (WUE). In this review, we describe the molecular details of stomatal CO2 sensing by CO2/HCO3−-induced interaction of two protein kinases, the HIGH LEAF TEMPERATURE 1 Raf-like kinase and the MPK4/MPK12 mitogen-activated protein kinases. The evolutionary emergence of, physiological relevance of, and potential for improvement of WUE of plants via the stomatal CO2 response and open questions in this research field are discussed. 

Summary Plants integrate environmental stimuli to optimize photosynthesis vs water loss by controlling stomatal apertures. However, stomatal responses to temperature elevation and the underlying molecular genetic mechanisms remain less studied.We developed an approach for clamping leaf‐to‐air vapor pressure difference (VPD_leaf) to fixed values, and recorded robust reversible warming‐induced stomatal opening in intact plants. We analyzed stomatal temperature responses of mutants impaired in guard cell signaling pathways for blue light, abscisic acid (ABA), CO₂, and the temperature‐sensitive proteins, Phytochrome B (phyB) and EARLY‐FLOWERING‐3 (ELF3).We confirmed thatphot1‐5/phot2‐1leaves lacking blue‐light photoreceptors showed partially reduced warming‐induced stomatal opening. Furthermore, ABA‐biosynthesis, phyB, and ELF3 were not essential for the stomatal warming response. Strikingly,Arabidopsis(dicot) andBrachypodium distachyon(monocot) mutants lacking guard cell CO₂sensors and signaling mechanisms, includinght1,mpk12/mpk4‐gc, andcbc1/cbc2abolished the stomatal warming response, suggesting a conserved mechanism across diverse plant lineages. Moreover, warming rapidly stimulated photosynthesis, resulting in a reduction in intercellular (CO₂). Interestingly, further enhancing heat stress caused stomatal opening uncoupled from photosynthesis.We provide genetic and physiological evidence that the stomatal warming response is triggered by increased CO₂assimilation and stomatal CO₂sensing. Additionally, increasing heat stress functions via a distinct photosynthesis‐uncoupled stomatal opening pathway. 

Stomatal pores close rapidly in response to low-air-humidity-induced leaf-to-air vapor pressure difference (VPD) increases, thereby reducing excessive water loss. The hydroactive signal-transduction mechanisms mediating high VPD–induced stomatal closure remain largely unknown. The kinetics of stomatal high-VPD responses were investigated by using time-resolved gas-exchange analyses of higher-order mutants in guard-cell signal-transduction branches. We show that the slow-type anion channel SLAC1 plays a relatively more substantial role than the rapid-type anion channel ALMT12/QUAC1 in stomatal VPD signaling. VPD-induced stomatal closure is not affected in mpk12 / mpk4GC double mutants that completely disrupt stomatal CO 2 signaling, indicating that VPD signaling is independent of the early CO 2 signal-transduction pathway. Calcium imaging shows that osmotic stress causes cytoplasmic Ca 2+ transients in guard cells. Nevertheless, osca1-2 / 1.3 / 2.2 / 2.3 / 3.1 Ca 2+ -permeable channel quintuple, osca1.3 / 1.7 -channel double, cngc5 / 6 -channel double, cngc20 -channel single, cngc19 / 20crispr -channel double, glr3.2 / 3.3 -channel double, cpk- kinase quintuple, cbl1 / 4 / 5 / 8 / 9 quintuple, and cbl2 / 3rf double mutants showed wild-type-like stomatal VPD responses. A B3-family Raf-like mitogen-activated protein (MAP)-kinase kinase kinase, M3Kδ5/RAF6, activates the OST1/SnRK2.6 kinase in plant cells. Interestingly, B3 Raf-kinase m3kδ5 and m3kδ1 / δ5 / δ6 / δ7 ( raf3 / 6 / 5 / 4 ) quadruple mutants, but not a 14-gene raf-kinase mutant including osmotic stress-linked B4-family Raf-kinases, exhibited slowed high-VPD responses, suggesting that B3-family Raf-kinases play an important role in stomatal VPD signaling. Moreover, high VPD–induced stomatal closure was impaired in receptor-like pseudokinase GUARD CELL HYDROGEN PEROXIDE-RESISTANT1 (GHR1) mutant alleles. Notably, the classical transient “wrong-way” VPD response was absent in ghr1 mutant alleles. These findings reveal genes and signaling mechanisms in the elusive high VPD–induced stomatal closing response pathway. 

Recent advances are revealing mechanisms mediating CO2-regulated stomatal movements in Arabidopsis, stomatal architecture and stomatal movements in grasses, and the long-term impact of CO2 on growth. 

Plant stomata sense CO2 via reversible interaction of the Raf-like HT1 protein kinase with non-activity requiring MAP kinase.