ACONITASE 3 is part of theANAC017 transcription factor-dependent mitochondrial dysfunction response

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 1...

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Published in:Plant physiology (Bethesda) 2021-08, Vol.186 (4), p.1859-1877
Main Authors: Pascual, Jesús, Rahikainen, Moona, Angeleri, Martina, Alegre, Sara, Gossens, Richard, Shapiguzov, Alexey, Heinonen, Arttu, Trotta, Andrea, Durian, Guido, Winter, Zsófia, Sinkkonen, Jari, Kangasjärvi, Jaakko, Whelan, James, Kangasjärvi, Saijaliisa
Format: Article
Language:English
Subjects:
Aconitate Hydratase - genetics
Aconitate Hydratase - metabolism
Arabidopsis - enzymology
Arabidopsis - genetics
Arabidopsis Proteins - genetics
Arabidopsis Proteins - metabolism
Mitochondria - metabolism
Transcription Factors - metabolism
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Summary: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'γ, 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 ACO3S91D-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.
ISSN:0032-0889
1532-2548
DOI:10.1093/plphys/kiab225