DELAY OF GERMINATION1 REQUIRES PP2C PHOSPHATASES OF THE ABA SIGNALING PATHWAY TO CONTROL SEED DORMANCY
Née, G.1,2, Kramer, K.3, Kazumi Nakabayashi, N.1, Yuan, B.1, Yong Xiang, Y.1,4, Emma Miatton, E.1, Iris Finkemeier, I.2,3 and Soppe, W.J.J.1,5
1Department of Plant Breeding and Genetics, Max Planck Institute for Plant Breeding Research, 50829 Cologne, Germany
2Institute of Plant Biology and Biotechnology, University of Münster, Schlossplatz 7, 48149 Münster, Germany
3Plant Proteomics, Max Planck Institute for Plant Breeding Research, Carl-von-Linné-Weg 10, 50829 Cologne, Germany
4Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences, 518120 Shenzhen, China
5Institute of Molecular Physiology and Biotechnology of Plants (IMBIO), University of Bonn, 53115 Bonn, Germany.
Contact : Guillaume Née, email@example.com
Seed germination is a major decision point in the life of plants determining future growth and development. This timing is controlled by seed dormancy, which prevents germination under favourable conditions. The plant hormone abscisic acid (ABA) and the protein DELAY OF GERMINATION 1 (DOG1) are essential regulators of dormancy. The function of ABA in dormancy is rather well understood, but the role of DOG1 is still unknown. The connection between ABA pathway and DOG1 pathway has been mentioned as an outstanding question in seed biology. Using affinity purification from functionally complemented dog1 lines and proteomics based methods, we identified more than 100 proteins that complex with DOG1 in seeds. Among them, we identified four phosphatases from which two belong to clade A of type 2C protein phosphatases: ABA-Hypersensitive Germination 1 (AHG1) and AHG3. BiFC interaction studies suggest that DOG1 interact specifically with a subset of PP2C including AHG1 that is specifically expressed in seeds and has been shown to be immune to inhibition by ABA and the ABA receptors of the PYR/PYL/RCAR family. Genetic analysis demonstrated that AHG1 and 3 have redundant but essential roles in the control of seed dormancy and that DOG1 works upstream of this phosphatases since the phenotype of the double ahg1 ahg3 mutant is fully epistatic to the phenotype of dog1 in a triple dog1 ahg1 ahg3 mutant. In addition, the genetic analysis indicates that DOG1 negatively influence the action of AHG1 and 3 regarding seed dormancy. We propose that the ABA and DOG1 dormancy pathways converge at clade A of type 2C protein phosphatases.