Abscisic acid (ABA) is an essential hormone for plants to survive environmental stresses. At the center of the ABA signaling network is a subfamily of type 2C protein phosphatases (PP2Cs), which form exclusive interactions with ABA receptors and subfamily 2 Snfl-related kinase (SnRK2s). Here, we report a SnRK2-PP2C complex structure, which reveals marked similarity in PP2C recognition by SnRK2 and ABA receptors. In the complex, the kinase activation loop docks into the active site of PP2C, while the conserved ABA-sensing tryptophan of PP2C inserts into the kinase catalytic cleft, thus mimicking receptor-PP2C interactions. These structural results provide a simple mechanism that directly couples ABA binding to SnRK2 kinase activation and highlight a new paradigm of kinase-phosphatase regulation through mutual packing of their catalytic sites.

Soil salinity is a major abiotic stress that decreases plant growth and productivity. Recently, it was reported that plants overexpressing AtNHX1 or SOS1 have significantly increased salt tolerance. To test whether overexpression of multiple genes can improve plant salt tolerance even more, we produced six different transgenic Arabidopsis plants that overexpress AtNHX1, SOS3, AtNHX1+SOS3, SOS1, SOS2+SOS3, or SOS1+SOS2+SOS3. Northern blot analyses confirmed the presence of high levels of the relevant gene transcripts in transgenic plants. Transgenic Arabidopsis plants overexpressing AtNHX1 alone did not present any significant increase in salt tolerance, contrary to earlier reports. We found that transgenic plants overexpressing SOS3 exhibit increased salt tolerance similar to plants overexpressing SOS1. Moreover, salt tolerance of transgenic plants overexpressing AtNHX1+SOS3, SOS2+SOS3, or SOS1+SOS2+SOS3, respectively, appeared similar to the tolerance of transgenic plants overexpressing either SOS1 or SOS3 alone.

The phytohormone abscisic acid (ABA) plays an important role in modulating plant growth, development, and stress responses. In a genetic screen for mutants with altered drought stress responses, we identified an ABA-overly sensitive mutant, the abo1 mutant, which showed a drought-resistant phenotype. The abo1 mutation enhances ABA-induced stomatal closing and increases ABA sensitivity in inhibiting seedling growth. abo1 mutants are more resistant to oxidative stress than the wild type and show reduced levels of transcripts of several stress-or ABA-responsive genes. Interestingly, the mutation also differentially modulates the development and growth of adjacent guard cells. Map-based cloning identified ABO1 as a new allele of ELO2, which encodes a homolog of Saccharomyces cerevisiae Iki3/Elp1/Tot1 and human IB kinase-associated protein. Water stress caused by drought and soil salinity is an important environmental factor that limits the productivity and distribution of plants. The cellular and molecular mechanisms of plant responses to water stress have been analyzed extensively (48,59,63). Water stress can induce the accumulation of the phytohormone abscisic acid (ABA) (59). ABA plays a vital role in triggering stomatal closure, which reduces transpirational water loss and constitutes an essential part of plant drought tolerance (48,58,63). Analysis of Arabidopsis thaliana mutants has defined several ABA response loci that encode proteins such as protein phosphatases and kinases, which greatly affect guard cell movement (10,45,58).Recent studies indicate that transcripts of protein-coding genes are regulated at all steps of RNA metabolism, from transcription initiation to RNA processing (50). A great deal of information about plant transcriptional regulators that bind the promoters to initiate gene transcription in response to water stress has been collected (61). In contrast, much less is known about proteins involved in RNA processing (30). Nevertheless, recent studies point to a central role of RNA processing in regulating ABA sensitivity and osmotic stress responses. The RNA-binding protein FCA was reported to be an ABA receptor, although it appears to function in ABA regulation of flowering rather than in seed dormancy or drought tolerance (44). ABH1, a cap-binding protein, functions in early ABA signaling (20). A recessive mutation in the SAD1 gene encoding an Sm-like snRNP required for mRNA splicing, export, and degradation rendered plants hypersensitive to ABA and drought (56). The Arabidopsis HYL1 gene encodes a nuclear double-stranded RNA-binding protein. A knockout mutation of the HYL1 gene caused abnormal development, increased sensitivity to abscisic acid, and reduced sensitivity to auxin and cytokinin (33). HYL1 controls gene expression likely through microRNA-mediated gene regulation, although the targeted genes related to ABA sensitivity are still unknown (18). AKIP1 isolated from Vicia faba is a single-stranded RNAbinding protein which can bind to a dehydrin mRNA after phosphorylation by an ABA-...