期刊
MOLECULAR PLANT
卷 6, 期 2, 页码 528-538出版社
CELL PRESS
DOI: 10.1093/mp/sss078
关键词
abscisic acid; ABA receptor; protein kinase; protein phosphatase; SLAC1
资金
- Biogreen21 Program Rural Development Administration [PJ008222]
- Research Foundation of Korea (NFR)
- Korea government [2011-0007600]
- US National Science Foundation
- Korean WCU Program of National Research Foundation
- National Research Foundation of Korea [2011-0007600] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Plant hormone abscisic acid (ABA) serves as an integrator of environmental stresses such as drought to trigger stomatal closure by regulating specific ion channels in guard cells. We previously reported that SLAC1, an outward anion channel required for stomatal closure, was regulated via reversible protein phosphorylation events involving ABA signaling components, including protein phosphatase 2C members and a SnRK2-type kinase (OST1). In this study, we reconstituted the ABA signaling pathway as a proteinprotein interaction relay from the PYL/RCAR-type receptors, to the PP2CSnRK2 phosphatasekinase pairs, to the ion channel SLAC1. The ABA receptors interacted with and inhibited PP2C phosphatase activity against the SnRK2-type kinase, releasing active SnRK2 kinase to phosphorylate, and activate the SLAC1 channel, leading to reduced guard cell turgor and stomatal closure. Both yeast two-hybrid and bimolecular fluorescence complementation assays were used to verify the interactions among the components in the pathway. These biochemical assays demonstrated activity modifications of phosphatases and kinases by their interaction partners. The SLAC1 channel activity was used as an endpoint readout for the strength of the signaling pathway, depending on the presence of different combinations of signaling components. Further study using transgenic plants overexpressing one of the ABA receptors demonstrated that changing the relative level of interacting partners would change ABA sensitivity.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据