Cell and Developmental Biology Section, Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093.
Graduate School of Environmental and Life Science, Okayama University, 7008530 Okayama, Japan.
Proc Natl Acad Sci U S A. 2018 Oct 16;115(42):E9971-E9980. doi: 10.1073/pnas.1809204115. Epub 2018 Oct 3.
Stomatal pore apertures are narrowing globally due to the continuing rise in atmospheric [CO]. CO elevation and the plant hormone abscisic acid (ABA) both induce rapid stomatal closure. However, the underlying signal transduction mechanisms for CO/ABA interaction remain unclear. Two models have been considered: () CO elevation enhances ABA concentrations and/or early ABA signaling in guard cells to induce stomatal closure and () CO signaling merges with ABA at OST1/SnRK2.6 protein kinase activation. Here we use genetics, ABA-reporter imaging, stomatal conductance, patch clamp, and biochemical analyses to investigate these models. The strong ABA biosynthesis mutants and remain responsive to CO elevation. Rapid CO-triggered stomatal closure in PYR/RCAR ABA receptor quadruple and hextuple mutants is not disrupted but delayed. Time-resolved ABA concentration monitoring in guard cells using a FRET-based ABA-reporter, ABAleon2.15, and ABA reporter gene assays suggest that CO elevation does not trigger [ABA] increases in guard cells, in contrast to control ABA exposures. Moreover, CO activates guard cell S-type anion channels in and ABA receptor hextuple mutants. Unexpectedly, in-gel protein kinase assays show that unlike ABA, elevated CO does not activate OST1/SnRK2 kinases in guard cells. The present study points to a model in which rapid CO signal transduction leading to stomatal closure occurs via an ABA-independent pathway downstream of OST1/SnRK2.6. Basal ABA signaling and OST1/SnRK2 activity are required to facilitate the stomatal response to elevated CO These findings provide insights into the interaction between CO/ABA signal transduction in light of the continuing rise in atmospheric [CO].
气孔孔径因大气中[CO]的持续升高而缩小。CO 升高和植物激素脱落酸（ABA）都能诱导气孔迅速关闭。然而，CO/ABA 相互作用的潜在信号转导机制尚不清楚。有两种模型被认为：（1）CO 升高增强了保卫细胞中的 ABA 浓度和/或早期 ABA 信号，以诱导气孔关闭；（2）CO 信号与 OST1/SnRK2.6 蛋白激酶激活处的 ABA 信号融合。在这里，我们使用遗传学、ABA 报告基因成像、气孔导度、膜片钳和生化分析来研究这些模型。强 ABA 生物合成突变体[CO]仍然对 CO 升高有反应。PYR/RCAR ABA 受体四重和六重突变体中快速 CO 触发的气孔关闭没有被破坏，只是被延迟。使用基于 FRET 的 ABA 报告基因，ABAleon2.15，和 ABA 报告基因分析，对保卫细胞中的快速 CO 触发的[ABA]浓度变化进行时间分辨监测，表明 CO 升高不会像对照 ABA 暴露那样引发保卫细胞中[ABA]的增加。此外，CO 激活了[CO]和 ABA 受体六重突变体中的保卫细胞 S 型阴离子通道。出乎意料的是，在凝胶蛋白激酶测定中，与 ABA 不同，升高的 CO 不会激活保卫细胞中的 OST1/SnRK2 激酶。本研究表明，在 OST1/SnRK2.6 下游，存在一种快速 CO 信号转导导致气孔关闭的 ABA 非依赖途径。基础 ABA 信号和 OST1/SnRK2 活性是促进气孔对 CO 升高的响应所必需的。这些发现为大气中[CO]持续升高背景下 CO/ABA 信号转导的相互作用提供了新的见解。
