Plant gas exchange is regulated by guard cells that form stomatal pores. Stomatal adjustments are crucial for plant survival; they regulate uptake of CO2 for photosynthesis, loss of water, and entrance of air pollutants such as ozone. We mapped ozone hypersensitivity, more open stomata, and stomatal CO2-insensitivity phenotypes of the Arabidopsis thaliana accession Cvi-0 to a single amino acid substitution in MITOGEN-ACTIVATED PROTEIN (MAP) KINASE 12 (MPK12). In parallel, we showed that stomatal CO2-insensitivity phenotypes of a mutant cis (CO2-insensitive) were caused by a deletion of MPK12. Lack of MPK12 impaired bicarbonate-induced activation of S-type anion channels. We demonstrated that MPK12 interacted with the protein kinase HIGH LEAF TEMPERATURE 1 (HT1)—a central node in guard cell CO2 signaling—and that MPK12 functions as an inhibitor of HT1. These data provide a new function for plant MPKs as protein kinase inhibitors and suggest a mechanism through which guard cell CO2 signaling controls plant water management.
Natural Variation in Arabidopsis Cvi-0 Accession Reveals an Important Role of MPK12 in Guard Cell CO2 Signaling
Liina Jakobson,L. Vaahtera,Kadri Tõldsepp,Maris Nuhkat,Cun Wang,Yuh-Shuh Wang,Hanna Hõrak,Ervin Valk,P. Pechter,Y. Sindarovska,Jing Tang,Chuanlei Xiao,Yanghong Xu,Ulvi Gerst Talas,A. García‐Sosa,Saijaliisa Kangasjärvi,U. Maran,M. Remm,M. Roelfsema,Honghong Hu,J. Kangasjärvi,M. Loog,J. Schroeder,H. Kollist,M. Brosché
Published 2016 in PLoS Biology
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- Publication year
2016
- Venue
PLoS Biology
- Publication date
2016-12-01
- Fields of study
Biology, Medicine, Environmental Science
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Semantic Scholar, PubMed
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