Graduate School of Life Science, Hokkaido University, Kita 10 Nishi 8, Kita-ku, Sapporo, Hokkaido, 060-0810 Japan.
Exploratory Research Center on Life and Living Systems (ExCELLS), 5-1 Higashiyama, Myodaiji, Okazaki, Aichi, 444-8787 Japan.
Plant Cell Physiol. 2020 May 1;61(5):942-956. doi: 10.1093/pcp/pcaa021.
Cell-to-cell communication is tightly regulated in response to environmental stimuli in plants. We previously used a photoconvertible fluorescent protein Dendra2 as a model reporter to study this process. This experiment revealed that macromolecular trafficking between protonemal cells in Physcomitrella patens is suppressed in response to abscisic acid (ABA). However, it remains unknown which ABA signaling components contribute to this suppression and how. Here, we show that ABA signaling components SUCROSE NON-FERMENTING 1-RELATED PROTEIN KINASE 2 (PpSnRK2) and ABA INSENSITIVE 3 (PpABI3) play roles as an essential and promotive factor, respectively, in regulating ABA-induced suppression of Dendra2 diffusion between cells (ASD). Our quantitative imaging analysis revealed that disruption of PpSnRK2 resulted in defective ASD onset itself, whereas disruption of PpABI3 caused an 81-min delay in the initiation of ASD. Live-cell imaging of callose deposition using aniline blue staining showed that, despite this onset delay, callose deposition on cross walls remained constant in the PpABI3 disruptant, suggesting that PpABI3 facilitates ASD in a callose-independent manner. Given that ABA is an important phytohormone to cope with abiotic stresses, we further explored cellular physiological responses. We found that the acquisition of salt stress tolerance is promoted by PpABI3 in a quantitative manner similar to ASD. Our results suggest that PpABI3-mediated ABA signaling may effectively coordinate cell-to-cell communication during the acquisition of salt stress tolerance. This study will accelerate the quantitative study for ABA signaling mechanism and function in response to various abiotic stresses.
细胞间通讯在植物中受到环境刺激的严格调控。我们之前使用光可转化的荧光蛋白 Dendra2 作为模型报告基因来研究这个过程。该实验表明，在Physcomitrella patens 中，质子细胞之间的大分子运输在受到脱落酸（ABA）时受到抑制。然而，目前尚不清楚哪些 ABA 信号成分对此抑制有贡献，以及如何贡献。在这里，我们表明 ABA 信号成分 SUCROSE NON-FERMENTING 1-RELATED PROTEIN KINASE 2（PpSnRK2）和 ABA INSENSITIVE 3（PpABI3）分别作为必需和促进因子，在调节 ABA 诱导的细胞间 Dendra2 扩散抑制（ASD）中发挥作用。我们的定量成像分析表明，PpSnRK2 的破坏导致 ASD 起始本身出现缺陷，而 PpABI3 的破坏导致 ASD 起始延迟 81 分钟。使用苯胺蓝染色对 callose 沉积的活细胞成像显示，尽管起始延迟，PpABI3 突变体中 cross walls 上的 callose 沉积仍然保持不变，表明 PpABI3 以 callose 非依赖的方式促进 ASD。鉴于 ABA 是应对非生物胁迫的重要植物激素，我们进一步探讨了细胞的生理反应。我们发现 PpABI3 以类似于 ASD 的方式促进了盐胁迫耐受性的获得。我们的结果表明，PpABI3 介导的 ABA 信号可能在获得盐胁迫耐受性期间有效地协调细胞间通讯。这项研究将加速对 ABA 信号机制及其对各种非生物胁迫反应的定量研究。
