Role of HT1 kinase in the CO₂ signal transduction pathway in guard cells

Abstract

Stomatal aperture is regulated by CO₂ concentration. CO₂ is converted to HCO₃^- by carbonic anhydrase (CA), and the HCO₃^- promotes H₂O₂ generation by NADPH oxidase in guard cells followed by stomatal closure. We previously isolated Arabidopsis mutant ht1 (high leaf temperature 1) which has a disrupted response to CO₂ but has normal responses to light and abscisic acid (ABA) in stomata. HT1 encodes a protein kinase that is expressed mainly in guard cells. These results suggest that HT1 kinase functions specifically in the CO₂ signal transduction pathway in guard cells, independent of the light and ABA signal transduction pathway. We examined the relations among HT1 kinase, production of HCO₃^- and H₂O₂ in the CO₂ signal transduction pathway in guard cells. ht1 had a normal response to H₂O₂ but had a disrupted response to HCO₃^-, and stomatal aperture was not restored by an NADPH oxidase inhibitor, DPI. These results raise the possibility that HT1 kinase is functioning downstream of CA, but does not have a significant effect on generating H₂O₂ by NADPH oxidase in the CO₂ signal transduction pathway in guard cells.