ACONITASE 3 is part of the ANAC017 transcription factor-dependent mitochondrial dysfunction response

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http://hdl.handle.net/10138/335630

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Pascual , J , Rahikainen , M , Angeleri , M , Alegre , S , Gossens , R , Shapiguzov , A , Heinonen , A , Trotta , A , Durian , G , Winter , Z , Sinkkonen , J , Kangasjarvi , J , Whelan , J & Kangasjärvi , S 2021 , ' ACONITASE 3 is part of the ANAC017 transcription factor-dependent mitochondrial dysfunction response ' , Plant Physiology , vol. 186 , no. 4 , pp. 1859-1877 . https://doi.org/10.1093/plphys/kiab225

Title: ACONITASE 3 is part of the ANAC017 transcription factor-dependent mitochondrial dysfunction response
Author: Pascual, Jesus; Rahikainen, Moona; Angeleri, Martina; Alegre, Sara; Gossens, Richard; Shapiguzov, Alexey; Heinonen, Arttu; Trotta, Andrea; Durian, Guido; Winter, Zsofia; Sinkkonen, Jari; Kangasjarvi, Jaakko; Whelan, James; Kangasjärvi, Saijaliisa
Contributor organization: Organismal and Evolutionary Biology Research Programme
Plant ROS-Signalling
Viikki Plant Science Centre (ViPS)
Plant Biology
Faculty of Biological and Environmental Sciences
Department of Agricultural Sciences
Crop Light
Date: 2021-08
Language: eng
Number of pages: 19
Belongs to series: Plant Physiology
ISSN: 0032-0889
DOI: https://doi.org/10.1093/plphys/kiab225
URI: http://hdl.handle.net/10138/335630
Abstract: Mitochondria are tightly embedded within metabolic and regulatory networks that optimize plant performance in response to environmental challenges. The best-known mitochondrial retrograde signaling pathway involves stress-induced activation of the transcription factor NAC DOMAIN CONTAINING PROTEIN 17 (ANAC017), which initiates protective responses to stress-induced mitochondrial dysfunction in Arabidopsis (Arabidopsis thaliana). Posttranslational control of the elicited responses, however, remains poorly understood. Previous studies linked protein phosphatase 2A subunit PP2A-B'gamma, a key negative regulator of stress responses, with reversible phosphorylation of ACONITASE 3 (ACO3). Here we report on ACO3 and its phosphorylation at Ser91 as key components of stress regulation that are induced by mitochondrial dysfunction. Targeted mass spectrometry-based proteomics revealed that the abundance and phosphorylation of ACO3 increased under stress, which required signaling through ANAC017. Phosphomimetic mutation at ACO3-Ser91 and accumulation of ACO3(S91D)-YFP promoted the expression of genes related to mitochondrial dysfunction. Furthermore, ACO3 contributed to plant tolerance against ultraviolet B (UV-B) or antimycin A-induced mitochondrial dysfunction. These findings demonstrate that ACO3 is both a target and mediator of mitochondrial dysfunction signaling, and critical for achieving stress tolerance in Arabidopsis leaves.
Subject: ALTERNATIVE OXIDASE
OXIDATIVE STRESS
GENE-EXPRESSION
PLANT
ARABIDOPSIS
IDENTIFICATION
METABOLISM
PP2A-B'GAMMA
RESISTANCE
INDUCTION
11831 Plant biology
Peer reviewed: Yes
Rights: cc_by
Usage restriction: openAccess
Self-archived version: publishedVersion


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