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

Kangasjärvi Saijaliisa; Rahikainen Moona; Pascual Jesús; Angeleri Martina; Winter Zsófia; Heinonen Arttu; Kangasjärvi Jaakko; Durian Guido; Trotta Andrea; Sinkkonen Jari; Alegre Sara; Whelan James; Shapiguzov Alexey; Gossens Richard

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

Kangasjärvi Saijaliisa
Rahikainen Moona
Pascual Jesús
Angeleri Martina
Winter Zsófia
Heinonen Arttu
Kangasjärvi Jaakko
Durian Guido
Trotta Andrea
Sinkkonen Jari
Alegre Sara
Whelan James
Shapiguzov Alexey
Gossens Richard
Katso/Avaa
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American Society of Plant Biologists
doi:10.1093/plphys/kiab225
URI
https://doi.org/10.1093/plphys/kiab225
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Julkaisun pysyvä osoite on:
https://urn.fi/URN:NBN:fi-fe2021120158434
Tiivistelmä

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). Post-translational 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 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.

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