Loss of the Acetyltransferase NAA50 Induces Endoplasmic Reticulum Stress and Immune Responses and Suppresses Growth
Stress signaling in plants is carefully regulated to ensure proper development and reproductive fitness. Overactive defense signaling can result in dwarfism as well as developmental defects. In addition to requiring a substantial amount of energy, plant stress responses place a burden upon the cellu...
Gespeichert in:
Veröffentlicht in: | Plant physiology (Bethesda) 2020-08, Vol.183 (4), p.1838-1854 |
---|---|
Hauptverfasser: | , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Stress signaling in plants is carefully regulated to ensure proper development and reproductive fitness. Overactive defense signaling can result in dwarfism as well as developmental defects. In addition to requiring a substantial amount of energy, plant stress responses place a burden upon the cellular machinery, which can result in the accumulation of misfolded proteins and endoplasmic reticulum (ER) stress. Negative regulators of stress signaling, such as
(
), ensure that stress responses are properly suspended when they are not needed, thereby conserving energy for growth and development. Here, we describe the role of an uncharacterized N-terminal acetyltransferase, NAA50, in the regulation of plant development and stress responses in Arabidopsis (
). Our results demonstrate that NAA50, an interactor of EDR1, plays an important role in regulating the tradeoff between plant growth and defense. Plants lacking
display severe developmental defects as well as induced stress responses. Reduction of
expression results in arrested stem and root growth as well as senescence. Furthermore, our results demonstrate that the loss of
results in constitutive ER stress signaling, indicating that
may be required for the suppression of ER stress. This work establishes
as essential for plant development and the suppression of stress responses, potentially through the regulation of ER stress. |
---|---|
ISSN: | 0032-0889 1532-2548 |
DOI: | 10.1104/pp.20.00225 |