Ethylene Signaling Enhances Mitochondrial Stress Tolerance Independently of the Transcription factor ANAC017 in Arabidopsis.

Mitochondria are central to plant metabolism, yet the diversity of mechanisms plants use to cope with mitochondrial stress and its implications in cellular signaling are not fully understood. In this study, we analyzed Arabidopsis noxy (nonresponding to oxylipins) mutants affected in 9-HOT (9(S)-hydroxy-10,12,15-octadecatrienoic acid) signaling, mitochondrial function and ethylene (ET) signaling to dissect plant responses to a range of mitochondrial stresses, including inhibitors of all electron transport chain complexes and mitochondrial translation. All noxy mutants showed resistance to antimycin A (AA), implicating Complex III and 9-HOT signaling in mitochondrial stress adaptation. Notably, noxy22/eto1-14, an ET overproducer mutant, displayed resistance to all tested inhibitors independently of the canonical mitochondrial retrograde pathway mediated by ANAC017. We found similar results in eto1-5 and eto1-13 alleles, thus sustaining a role for ET in mitochondrial protection. Histochemical and RNA-seq analysis revealed that AA induced ANAC017-regulated genes early and independently of ET signaling whereas EIN2 contributed in later induction of AA-associated immune responses. EIN2 was required for full activation of AA-induced resistance against the biotrophic pathogen Hyaloperonospora arabidopsidis, but not against the necrotroph Plectosphaerella cucumerina. Collectively, our findings point to a complex network that coordinates distinct but overlapping responses to mitochondrial dysfunction and integrates them into broader stress pathways.