TMK1-based auxin signaling regulates abscisic acid responses via phosphorylating ABI1/2 in Arabidopsis.

Differential concentrations of phytohormone trigger distinct outputs, which provides a mechanism for the plasticity of plant development and an adaptation strategy among plants to changing environments. However, the underlying mechanisms of the differential responses remain unclear. Here we report that a high concentration of auxin, distinct from the effect of low auxin concentration, enhances abscisic acid (ABA) responses in Arabidopsis thaliana, which partially relies on TRANS-MEMBERANE KINASE 1 (TMK1), a key regulator in auxin signaling. We show that high auxin and TMK1 play essential and positive roles in ABA signaling through regulating ABA INSENSITIVE 1 and 2 (ABI1/2), two negative regulators of the ABA pathway. TMK1 inhibits the phosphatase activity of ABI2 by direct phosphorylation of threonine 321 (T321), a conserved phosphorylation site in ABI2 proteins, whose phosphorylation status is important for both auxin and ABA responses. This TMK1-dependent auxin signaling in the regulation of ABA responses provides a possible mechanism underlying the high auxin responses in plants and an alternative mechanism involved in the coordination between auxin and ABA signaling.

The involvement of abscisic acid-insensitive mutants in low phosphate stress responses during rhizosphere acidification, anthocyanin accumulation and Pi homeostasis in Arabidopsis.

Phosphorus is an essential plant nutrient, used in the formation of macromolecules such as nucleic acids and phospholipids. Abscisic acid (ABA) may be involved in the process of low inorganic phosphate (Pi) responses. The phenotypes of ABA-insensitive Arabidopsis mutants (abi1/2/3/4/5) under low Pi stress were investigated to identify possible low Pi response mutant genes. The results showed enhanced rhizosphere acidification in the abi1-1/abi2-1/abi5-1 mutants under low Pi stress compared with wild-type (WT) seedlings. The abi1-1/abi2-1/ abi3-1/abi5-1 mutants accumulated less anthocyanin than the WT, while the abi4-1 mutant showed greater accumulation, implicating all the ABA-insensitive mutants in anthocyanin deposition under Pi deficiency. Alterations in the Pi contents of roots or shoots were also observed in the mutants in response to both Pi sufficiency and deficiency, indicating that the mutants were involved in Pi uptake or transportation. The primary root length and root-shoot ratio of abi3-1 and abi4-1 mutants decreased compared with WT seedlings under low Pi condition. Further research showed that ABI5 could regulate PHT1;5 and WRKY42 expression by combining with ACGT cis-acting elements of the PHT1;5 and WRKY42 promoters.

Rheostatic Control of ABA Signaling through HOS15-Mediated OST1 Degradation.

Dehydrating stresses trigger the accumulation of abscisic acid (ABA), a key plant stress-signaling hormone that activates Snf1-Related Kinases (SnRK2s) to mount adaptive responses. However, the regulatory circuits that terminate the SnRK2s signal relay after acclimation or post-stress conditions remain to be defined. Here, we show that the desensitization of the ABA signal is achieved by the regulation of OST1 (SnRK2.6) protein stability via the E3-ubiquitin ligase HOS15. Upon ABA signal, HOS15-induced degradation of OST1 is inhibited and stabilized OST1 promotes the stress response. When the ABA signal terminates, protein phosphatases ABI1/2 promote rapid degradation of OST1 via HOS15. Notably, we found that even in the presence of ABA, OST1 levels are also depleted within hours of ABA signal onset. The unexpected dynamics of OST1 abundance are then resolved by systematic mathematical modeling, demonstrating a desensitizing feedback loop by which OST1-induced upregulation of ABI1/2 leads to the degradation of OST1. This model illustrates the complex rheostat dynamics underlying the ABA-induced stress response and desensitization.