The HT1 protein kinase is essential for red light‐induced stomatal opening and genetically interacts with OST1 in red light and CO2‐induced stomatal movement responses

Summary 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].