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

Abstract

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].