
The phytohormone abscisic acid (ABA) regulates plant growth, development and responses to biotic and abiotic stresses. The core ABA signaling pathway consists of three major components: ABA receptor (PYR1/PYLs), type 2C Protein Phosphatase (PP2C) and SNF1-related protein kinase 2 (SnRK2). Nevertheless, the complexity of ABA signaling remains to be explored. To uncover new components of ABA signal transduction pathways, we performed a yeast two-hybrid screen for SnRK2-interacting proteins. We found that Type One Protein Phosphatase 1 (TOPP1) and its regulatory protein, At Inhibitor-2 (AtI-2), physically interact with SnRK2s and also with PYLs. TOPP1 inhibited the kinase activity of SnRK2.6, and this inhibition could be enhanced by AtI-2. Transactivation assays showed that TOPP1 and AtI-2 negatively regulated the SnRK2.2/3/6-mediated activation of the ABA responsive reporter gene RD29B, supporting a negative role of TOPP1 and AtI-2 in ABA signaling. Consistent with these findings, topp1 and ati-2 mutant plants displayed hypersensitivities to ABA and salt treatments, and transcriptome analysis of TOPP1 and AtI-2 knockout plants revealed an increased expression of multiple ABA-responsive genes in the mutants. Taken together, our results uncover TOPP1 and AtI-2 as negative regulators of ABA signaling.
570, Arabidopsis Proteins, Arabidopsis, Membrane Transport Proteins, xxx, QH426-470, Protein Serine-Threonine Kinases, Plants, Genetically Modified, Plant Roots, Gene Expression Regulation, Plant, Seedlings, Protein Phosphatase 1, Genetics, Cold Shock Proteins and Peptides, Phosphoprotein Phosphatases, Protein Kinases, Research Article, Abscisic Acid, Signal Transduction
570, Arabidopsis Proteins, Arabidopsis, Membrane Transport Proteins, xxx, QH426-470, Protein Serine-Threonine Kinases, Plants, Genetically Modified, Plant Roots, Gene Expression Regulation, Plant, Seedlings, Protein Phosphatase 1, Genetics, Cold Shock Proteins and Peptides, Phosphoprotein Phosphatases, Protein Kinases, Research Article, Abscisic Acid, Signal Transduction
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