CAD1 contributes to osmotic tolerance in Arabidopsis thaliana by suppressing immune responses under osmotic stress.

Acquired osmotolerance Osmotic stress response

Journal

Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516

Informations de publication

Date de publication:
03 May 2024
Historique:
received: 30 04 2024
accepted: 01 05 2024
medline: 8 5 2024
pubmed: 8 5 2024
entrez: 7 5 2024
Statut: aheadofprint

Résumé

Acquired osmotolerance induced by initial exposure to mild salt stress is widespread across Arabidopsis thaliana ecotypes, but the mechanism underlying it remains poorly understood. To clarify it, we isolated acquired osmotolerance-deficient 1 (aod1), a mutant highly sensitive to osmotic stress, from ion-beam-irradiated seeds of Zu-0, an ecotype known for its remarkably high osmotolerance. Aod1 showed growth inhibition with spotted necrotic lesions on the rosette leaves under normal growth conditions on soil. However, its tolerance to salt and oxidative stresses was similar to that of the wild type (WT). Genetic and genome sequencing analyses suggested that the gene causing aod1 is identical to CONSTITUTIVELY ACTIVATED CELL DEATH 1 (CAD1). Complementation with the WT CAD1 gene restored the growth and osmotolerance of aod1, indicating that mutated CAD1 is responsible for the observed phenotypes in aod1. Although CAD1 is known to act as a negative regulator of immune response, transcript levels in the WT increased in response to osmotic stress. Aod1 displayed enhanced immune response and cell death under normal growth conditions, whereas the expression profiles of osmotic response genes were comparable to those of the WT. These findings suggest that autoimmunity in aod1 is detrimental to osmotolerance. Overall, our results suggest that CAD1 negatively regulates immune responses under osmotic stress, contributing to osmotolerance in Arabidopsis.

Identifiants

pubmed: 38714014
pii: S0006-291X(24)00585-0
doi: 10.1016/j.bbrc.2024.150049
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

150049

Informations de copyright

Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Yusuke Murakoshi (Y)

Department of Bioscience, Tokyo University of Agriculture, Tokyo, 156-8502, Japan.

Yasutaka Saso (Y)

Department of Bioscience, Tokyo University of Agriculture, Tokyo, 156-8502, Japan.

Minamo Matsumoto (M)

Department of Bioscience, Tokyo University of Agriculture, Tokyo, 156-8502, Japan.

Kazuha Yamanaka (K)

Department of Bioscience, Tokyo University of Agriculture, Tokyo, 156-8502, Japan.

Izumi Yotsui (I)

Department of Bioscience, Tokyo University of Agriculture, Tokyo, 156-8502, Japan.

Yoichi Sakata (Y)

Department of Bioscience, Tokyo University of Agriculture, Tokyo, 156-8502, Japan.

Teruaki Taji (T)

Department of Bioscience, Tokyo University of Agriculture, Tokyo, 156-8502, Japan. Electronic address: t3teruak@nodai.ac.jp.

Classifications MeSH