Stomatal CO<sub>2</sub>/bicarbonate sensor consists of two interacting protein kinases, Raf-like HT1 and non-kinase-activity requiring MPK12/MPK4.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 36475789.
- Also identified by DOI 10.1126/sciadv.abq6161 and PMC identifier 9728965.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
The continuing rise in the atmospheric carbon dioxide (CO<sub>2</sub>) concentration causes stomatal closing, thus critically affecting transpirational water loss, photosynthesis, and plant growth. However, the primary CO<sub>2</sub> sensor remains unknown. Here, we show that elevated CO<sub>2</sub> triggers interaction of the MAP kinases MPK4/MPK12 with the HT1 protein kinase, thus inhibiting HT1 kinase activity. At low CO<sub>2</sub>, HT1 phosphorylates and activates the downstream negatively regulating CBC1 kinase. Physiologically relevant HT1-mediated phosphorylation sites in CBC1 are identified. In a genetic screen, we identify dominant active HT1 mutants that cause insensitivity to elevated CO<sub>2</sub>. Dominant HT1 mutants abrogate the CO<sub>2</sub>/bicarbonate-induced MPK4/12-HT1 interaction and HT1 inhibition, which may be explained by a structural AlphaFold2- and Gaussian-accelerated dynamics-generated model. Unexpectedly, MAP kinase activity is not required for CO<sub>2</sub> sensor function and CO<sub>2</sub>-triggered HT1 inhibition and stomatal closing. The presented findings reveal that MPK4/12 and HT1 together constitute the long-sought primary stomatal CO<sub>2</sub>/bicarbonate sensor upstream of the CBC1 kinase in plants.