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. 2017 Oct 30;8:1183. doi: 10.1038/s41467-017-01239-3

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — AMFs are potent PYL receptor agonists. a–d Agonist dose–response curves for AMFs and AMC1β. Dose-dependent interactions between HAB1 and PYR1 (a), PYL1 (b), PYL2 (c), or PYL7 (d) in the presence of all five AMFs, AMC1β, AM1 and (+)-ABA are determined in AlphaScreen assays. EC₅₀ values for the interactions are listed below the curves (n = 3, error bars = SD). e Inhibition of HAB1 activity induced by AMFs and mediated by the 11 PYLs in phosphatase activity assays. The working concentration is 1 μM for AMF1β, AMF2α, and (+)-ABA. Values are means ± SD (n = 3). f Dose-dependent inhibition of HAB1 activity resulting from the binding of AMFs to the PYL2–HAB1 complex. The working concentrations are 1 and 0.1 μM for all five AMFs and (+)-ABA. Values are means ± SD (n = 3)