Abstract
Increasing carbon dioxide (CO₂) levels in the atmosphere have caused global metabolic changes in diverse plant species. CO₂ is not only a carbon donor for photosynthesis but also an environmental signal that regulates stomatal movements and thereby controls plant-water relationships and carbon metabolism. However, the mechanism underlying CO₂ sensing in stomatal guard cells remains unclear. Here we report characterization of Arabidopsis RESISTANT TO HIGH CO₂ (RHC1), a MATE-type transporter that links elevated CO₂ concentration to repression of HT1, a protein kinase that negatively regulates CO₂-induced stomatal closing. We also show that HT1 phosphorylates and inactivates OST1, a kinase which is essential for the activation of the SLAC1 anion channel and stomatal closing. Combining genetic, biochemical and electrophysiological evidence, we reconstituted the molecular relay from CO₂ to SLAC1 activation, thus establishing a core pathway for CO₂ signalling in plant guard cells.
Highlights
Increasing carbon dioxide (CO2) levels in the atmosphere have caused global metabolic changes in diverse plant species
We further demonstrate that RHC1 serves as an upstream regulator of HT1 that in turn inhibits OST1, connecting the CO2-specific pathway to OST1– SLAC1 activation, a common step shared by the abscisic acid (ABA) and CO2 responses
Because membrane transporters play an important role in modulating stomatal response to external signals[5,6,14,15,16,38,39,40], we hypothesized that mutations in many of such transporters may affect stomatal responses to environmental signals including CO2 concentration
Summary
Increasing carbon dioxide (CO2) levels in the atmosphere have caused global metabolic changes in diverse plant species. The mechanism underlying CO2 sensing in stomatal guard cells remains unclear. Stomatal pores are responsible for gas exchange between plants and the atmosphere, thereby controlling plant–water relationships and carbon metabolism. Elevated CO2 concentration activates anion channels, resulting in depolarization of plasma membrane in guard cells, causing efflux of solutes and stomatal closure[7,8,9,10]. Earlier studies in Arabidopsis identified several mutants with defects in CO2-induced stomatal movements[11,12,13,14,15,16,17,18,19] Most of these mutants including abi[1], abi[], gca[2], ost[1] and slac[1] were insensitive to both
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