RT Journal Article
SR Electronic
T1 Natural Variation in Arabidopsi<em>s</em> Cvi-0 Accession Uncovers Regulation of Guard Cell CO<sub>2</sub> Signaling by MPK12
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 073015
DO 10.1101/073015
A1 Liina Jakobson
A1 Lauri Vaahtera
A1 Kadri Tõldsepp
A1 Maris Nuhkat
A1 Cun Wang
A1 Yuh-Shuh Wang
A1 Hanna Hõrak
A1 Ervin Valk
A1 Priit Pechter
A1 Yana Sindarovska
A1 Jing Tang
A1 Chuanlei Xiao
A1 Yang Xu
A1 Ulvi Gerst Talas
A1 Maido Remm
A1 Saijaliisa Kangasjärvi
A1 M. Rob G. Roelfsema
A1 Honghong Hu
A1 Jaakko Kangasjärvi
A1 Mart Loog
A1 Julian I. Schroeder
A1 Hannes Kollist
A1 Mikael Brosché
YR 2016
UL http://biorxiv.org/content/early/2016/09/01/073015.abstract
AB 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 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 HT1, a central node in guard cell CO2 signaling, and that MPK12 can function 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.