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The question of whether red light‐induced stomatal opening is mediated by a photosynthesis‐derived reduction in intercellular [CO₂] (Cᵢ) remains controversial and genetic analyses are needed. The Arabidopsis thaliana protein kinase HIGH TEMPERATURE 1 (HT1) is a negative regulator of [CO₂]‐induced stomatal closing and ht1‐2 mutant plants do not show stomatal opening to low [CO₂]. The protein kinase mutant ost1‐3 exhibits slowed stomatal responses to CO₂. The functions of HT1 and OPEN STOMATA 1 (OST1) to changes in red, blue light or [CO₂] were analyzed. For comparison we assayed recessive ca1ca4 carbonic anhydrase double mutant plants, based on their slowed stomatal response to CO₂. Here, we report a strong impairment in ht1 in red light‐induced stomatal opening whereas blue light was able to induce stomatal opening. The effects on photosynthetic performance in ht1 were restored when stomatal limitation of CO₂ uptake, by control of [Cᵢ], was eliminated. HT1 was found to interact genetically with OST1 both during red light‐ and low [CO₂]‐induced stomatal opening. Analyses of ca1ca4 plants suggest that more than a low [Cᵢ]‐dependent pathway may function in red light‐induced stomatal opening. These results demonstrate that HT1 is essential for red light‐induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO₂].

It has been reported that stomatal conductance often limits the steady-state photosynthetic rate. On the other hand, the stomatal limitation of photosynthesis in fluctuating light remains largely unknown, although in nature light fluctuates due to changes in sun position, cloud cover, and the overshadowing canopy. In this study, we analysed three mutant lines of Arabidopsis with increased stomatal conductance to examine to what extent stomatal opening limits photosynthesis in fluctuating light. The slac1 (slow anion channel-associated 1) and ost1 (open stomata 1) mutants with stay-open stomata, and the PATROL1 (proton ATPase translocation control 1) overexpression line with faster stomatal opening responses exhibited higher photosynthetic rates and plant growth in fluctuating light than the wildtype, whereas these four lines showed similar photosynthetic rates and plant growth in constant light. The slac1 and ost1 mutants tended to keep their stomata open in fluctuating light, resulting in lower water-use efficiency (WUE) than the wild-type. However, the PATROL1 overexpression line closed stomata when needed and opened stomata immediately upon irradiation, resulting in similar WUE to the wild-type. The present study clearly shows that there is room to optimize stomatal responses, leading to greater photosynthesis and biomass accumulation in fluctuating light in nature.

The rate of gas exchange in plants is regulated mainly by stomatal size and density. Generally, higher densities of smaller stomata are advantageous for gas exchange; however, it is unclear what the effect of an extraordinary change in stomatal size might have on a plant's gas-exchange capacity. We investigated the stomatal responses to CO₂ concentration changes among 374 Arabidopsis (Arabidopsis thaliana) ecotypes and discovered that Mechtshausen (Me-0), a natural tetraploid ecotype, has significantly larger stomata and can achieve a high stomatal conductance. We surmised that the cause of the increased stomatal conductance is tetraploidization; however, the stomatal conductance of another tetraploid accession, tetraploid Columbia (Col), was not as high as that in Me-0. One difference between these two accessions was the size of their stomatal apertures. Analyses of abscisic acid sensitivity, ion balance, and gene expression profiles suggested that physiological or genetic factors restrict the stomatal opening in tetraploid Col but not in Me-0. Our results show that Me-0 overcomes the handicap of stomatal opening that is typical for tetraploids and achieves higher stomatal conductance compared with the closely related tetraploid Col on account of larger stomatal apertures. This study provides evidence for whether larger stomatal size in tetraploids of higher plants can improve stomatal conductance.

Stomata are small pores surrounded by guard cells that regulate gas exchange between plants and the atmosphere. Guard cells integrate multiple environmental signals and control the aperture width to ensure appropriate stomatal function for plant survival. Leaf temperature can be used as an indirect indicator of stomatal conductance to environmental signals. In this study, leaf thermal imaging of 374 Arabidopsis ecotypes was performed to assess their stomatal responses to changes in environmental CO2 concentrations. We identified three ecotypes, Köln (Kl-4), Gabelstein (Ga-0), and Chisdra (Chi-1), that have particularly low responsiveness to changes in CO2 concentrations. We next investigated stomatal responses to other environmental signals in these selected ecotypes, with Col-0 as the reference. The stomatal responses to light were also reduced in the three selected ecotypes when compared with Col-0. In contrast, their stomatal responses to changes in humidity were similar to those of Col-0. Of note, the responses to abscisic acid, a plant hormone involved in the adaptation of plants to reduced water availability, were not entirely consistent with the responses to humidity. This study demonstrates that the stomatal responses to CO2 and light share closely associated signaling mechanisms that are not generally correlated with humidity signaling pathways in these ecotypes. The results might reflect differences between ecotypes in intrinsic response mechanisms to environmental signals.

Specific cellular components including products of phosphatidylinositol (PI) metabolism play an important role as signaling molecules in stomatal responses to environmental signals. In this study, pharmacological inhibitors of a set of cellular components, including PI4-kinase (PI4K) and PI3K, were used to investigate stomatal closure in response to CO , darkness, and abscisic acid (ABA). Treatment with PAO, a specific inhibitor of PI4K, specifically inhibited the stomatal response to CO compared with that to darkness and ABA. In contrast, treatment with LY294002, a PI3K-specific inhibitor, specifically inhibited the stomatal response to darkness compared with that to CO and ABA. The specific inhibitory effects of PAO and LY294002 were also observed as changes in the spatial density of dot-like structures labeled by green fluorescent protein-tagged PATROL1, a protein that controls stomatal aperture possibly via regulation of H -ATPase amount in guard cell plasma membranes. Our results suggest an important role for PI4K and PI3K in the CO and darkness signal transduction pathways, respectively, that mediate PATROL1 dynamics.

Main conclusionPATOL1 contributes to increasing biomass not only by effective stomatal movement but also by root meristematic activity.PATROL1 (PROTON ATPase TRANSLOCATION CONTROL 1), a protein with a MUN domain, is involved in the intercellular trafficking of AHA1 H+-ATPase to the plasma membrane in guard cells. This allows for larger stomatal opening and more efficient photosynthesis, leading to increased biomass. Although PATROL1 is expressed not only in stomata but also in other tissues of the shoot and root, the role in other tissues than stomata has not been determined yet. Here, we investigated PATROL1 functions in roots using a loss-of-function mutant and an overexpressor. Cytological observations revealed that root meristematic size was significantly smaller in the mutant resulting in the short primary root. Grafting experiments showed that the shoot biomass of the mutant scion was increased when it grafted onto wild-type or overexpressor rootstocks. Conversely, grafting of the overexpressor scion shoot enhanced the growth of the mutant rootstock. The leaf temperatures of the grafted plants were consistent with those of their respective genotypes, indicating cell-autonomous behavior of stomatal movement and independent roles of PATROL1 in plant growth. Moreover, plasma membrane localization of AHA1 was not altered in root epidermal cells in the patrol1 mutant implying existence of a different mode of PATROL1 action in roots. Thus PATROL1 plays a role in root meristem and contributes to increase shoot biomass.

HT1 (HIGH LEAF TEMPERATURE 1) is the first component associated with changes in stomatal aperture in response to CO₂ to be isolated by forward genetic screening. The HT1 gene encodes a protein kinase expressed mainly in guard cells. The loss-of-function ht1-1 and ht1-2 mutants in Arabidopsis thaliana have CO₂-hypersensitive stomatal closure with concomitant reductions in their kinase activities in vitro. In addition to these mutants, in this study we isolate or obtaine five new ht1 alleles (ht1-3, ht1-4, ht1-5, ht1-6, and ht1-7). Among the mutants, only ht1-3 has a dominant mutant phenotype and has widely opened stomata due to CO₂ insensitivity. The ht1-3 mutant has a missense mutation affecting a non-conserved residue (R102K), whereas the other six recessive mutants have mutations in highly conserved residues in the catalytic domains required for kinase activity. We found that the dominant mutation does not affect the expression of HT1 or the ability to phosphorylate casein, a universal kinase substrate, but it does affect autophosphorylation activity in vitro. A 3D structural model of HT1 also shows that the R102 residue protrudes from the surface of the kinase, implying a role for the formation of oligomers and/or interaction with its targets. We demonstrate that both the loss-of-function and gain-of-function ht1 mutants have completely disrupted CO₂ responses, although they have normal responses to ABA. Furthermore, light-induced stomatal opening is smaller in ht1-3 and much smaller in ht1-2. Taken together, these results indicate that HT1 is a critical regulator for CO₂ signaling and is partially involved in the light-induced stomatal opening pathway.

Plants control CO 2 uptake and water loss by modulating the aperture of stomata located in the epidermis. Stomatal opening is initiated by the activation of H + -ATPases in the guard-cell plasma membrane. In contrast to regulation of H + -ATPase activity, little is known about the translocation of the guard cell H + -ATPase to the plasma membrane. Here we describe the isolation of an Arabidopsis gene, PATROL1 , that controls the translocation of a major H + -ATPase, AHA1, to the plasma membrane. PATROL1 encodes a protein with a MUN domain, known to mediate synaptic priming in neuronal exocytosis in animals. Environmental stimuli change the localization of plasma membrane-associated PATROL1 to an intracellular compartment. Plasma membrane localization of AHA1 and stomatal opening require the association of PATROL1 with AHA1. Increased stomatal opening responses in plants overexpressing PATROL1 enhance the CO 2 assimilation rate, promoting plant growth. In plants, stomatal opening controls the uptake of carbon dioxide and water loss, and is controlled by an H + ATPase. This study reports the identification of PATROL1, a gene that controls the subcellular localisation of the H + ATPase, and is involved in the regulation of stomata.

Highlight Loss-of-function and gain-of-function ht1 Arabidopsis mutants have completely disrupted CO sub(2) responses due to reduced and enhanced kinase activities, respectively.HT1 (HIGH LEAF TEMPERATURE 1) is the first component associated with changes in stomatal aperture in response to CO sub(2) to be isolated by forward genetic screening. The HT1 gene encodes a protein kinase expressed mainly in guard cells. The loss-of-function ht1-1 and ht1-2 mutants in Arabidopsis thaliana have CO sub(2)-hypersensitive stomatal closure with concomitant reductions in their kinase activities in vitro. In addition to these mutants, in this study we isolate or obtaine five new ht1 alleles (ht1-3, ht1-4, ht1-5, ht1-6, and ht1-7). Among the mutants, only ht1-3 has a dominant mutant phenotype and has widely opened stomata due to CO sub(2) insensitivity. The ht1-3 mutant has a missense mutation affecting a non-conserved residue (R102K), whereas the other six recessive mutants have mutations in highly conserved residues in the catalytic domains required for kinase activity. We found that the dominant mutation does not affect the expression of HT1 or the ability to phosphorylate casein, a universal kinase substrate, but it does affect autophosphorylation activity in vitro. A 3D structural model of HT1 also shows that the R102 residue protrudes from the surface of the kinase, implying a role for the formation of oligomers and/or interaction with its targets. We demonstrate that both the loss-of-function and gain-of-function ht1 mutants have completely disrupted CO sub(2) responses, although they have normal responses to ABA. Furthermore, light-induced stomatal opening is smaller in ht1-3 and much smaller in ht1-2. Taken together, these results indicate that HT1 is a critical regulator for CO sub(2) signaling and is partially involved in the light-induced stomatal opening pathway.