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 Jakobson, Liina
A1 Vaahtera, Lauri
A1 Tõldsepp, Kadri
A1 Nuhkat, Maris
A1 Wang, Cun
A1 Wang, Yuh-Shuh
A1 Hõrak, Hanna
A1 Valk, Ervin
A1 Pechter, Priit
A1 Sindarovska, Yana
A1 Tang, Jing
A1 Xiao, Chuanlei
A1 Xu, Yang
A1 Gerst Talas, Ulvi
A1 Remm, Maido
A1 Kangasjärvi, Saijaliisa
A1 Roelfsema, M. Rob G.
A1 Hu, Honghong
A1 Kangasjärvi, Jaakko
A1 Loog, Mart
A1 Schroeder, Julian I.
A1 Kollist, Hannes
A1 Brosché, Mikael
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.