Journal
NEW PHYTOLOGIST
Volume 208, Issue 4, Pages 1126-1137Publisher
WILEY
DOI: 10.1111/nph.13566
Keywords
Arabidopsis thaliana; HIGH TEMPERATURE 1 (HT1); low [CO2]; OPEN STOMATA 1 (OST1); photosynthesis; red light; stomata
Categories
Funding
- Swedish Research Council Formas
- Swedish Innovation Agency Vinnova
- National Science Foundation [MCB1414339]
- Ministry of Education, Culture, Sports, Science and Technology of Japan [21114002, 26221103]
- JC Kempe Foundation
- JOD Olsson Foundation
- Swedish University of Agricultural Sciences
- Direct For Biological Sciences
- Div Of Molecular and Cellular Bioscience [1414339] Funding Source: National Science Foundation
- Grants-in-Aid for Scientific Research [26221103] Funding Source: KAKEN
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The question of whether red light-induced stomatal opening is mediated by a photosynthesis-derived reduction in intercellular [CO2] (C-i) 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 [C-i], 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 [C-i]-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].
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