Abstract
Recent identification of the soluble ABA receptors, PYR/PYL/RCAR1,2), made a great progress in our understanding of ABA signaling. The receptor inhibits protein phosphatase 2C (PP2C), a major negative regulator of ABA response, in an ABA-dependent manner. On the other hand, our group have studied in planta or molecular functions of PP2C or the SNF1-related protein kinase 2 (SnRK2) for long years. In this study, we demonstrated that 1) SnRK2 functions as a central hub in ABA signaling network, 2) SnRK2 and PP2C interact in various combinations, and 3) PP2C inactivates SnRK2 by direct dephosphorylation3). In addition, three subclass III SnRK2s phosphorylate and activate bZIP transcription factors AREB/ABF/ABI5, major regulators of ABA-responsive gene expression. Combining these results, the ABA signal transduction pathway can be simplified to just 4 steps of signaling processes from perception to gene expression3). We also showed that abi1-1-type mutation of PP2C constitutively inactivate SnRK2s, and solved a long-standing mystery of ABA insensitivity of abi1-1 mutant3).
References: 1) Ma et al. (2009) Science, 2) Park et al. (2009) Science, 3) Umezawa et al. (2009) PNAS
