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Reciprocal Regulation of the TOR Kinase and ABA Receptor Balances Plant Growth and Stress Response.
- Source :
-
Molecular cell [Mol Cell] 2018 Jan 04; Vol. 69 (1), pp. 100-112.e6. Date of Electronic Publication: 2017 Dec 28. - Publication Year :
- 2018
-
Abstract
- As sessile organisms, plants must adapt to variations in the environment. Environmental stress triggers various responses, including growth inhibition, mediated by the plant hormone abscisic acid (ABA). The mechanisms that integrate stress responses with growth are poorly understood. Here, we discovered that the Target of Rapamycin (TOR) kinase phosphorylates PYL ABA receptors at a conserved serine residue to prevent activation of the stress response in unstressed plants. This phosphorylation disrupts PYL association with ABA and with PP2C phosphatase effectors, leading to inactivation of SnRK2 kinases. Under stress, ABA-activated SnRK2s phosphorylate Raptor, a component of the TOR complex, triggering TOR complex dissociation and inhibition. Thus, TOR signaling represses ABA signaling and stress responses in unstressed conditions, whereas ABA signaling represses TOR signaling and growth during times of stress. Plants utilize this conserved phospho-regulatory feedback mechanism to optimize the balance of growth and stress responses.<br /> (Copyright © 2017 Elsevier Inc. All rights reserved.)
- Subjects :
- Phosphorylation
Protein Serine-Threonine Kinases metabolism
Regulatory-Associated Protein of mTOR metabolism
Signal Transduction
Stress, Physiological
Abscisic Acid metabolism
Arabidopsis growth & development
Arabidopsis Proteins metabolism
Gene Expression Regulation, Plant physiology
Phosphatidylinositol 3-Kinases metabolism
Plant Growth Regulators metabolism
Receptors, Cell Surface metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1097-4164
- Volume :
- 69
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Molecular cell
- Publication Type :
- Academic Journal
- Accession number :
- 29290610
- Full Text :
- https://doi.org/10.1016/j.molcel.2017.12.002