Ethylene Signaling Enhances Mitochondrial Stress Tolerance Independently of ANAC017 in Arabidopsis

Mitochondria are central to plant metabolism, yet the diversity of mechanisms plants use to cope with mitochondrial stress and its implications as a cellular signal are not fully understood. In this study, we analyzed Arabidopsis noxy (non-responding to oxylipins) mutants affected in mitochondrial function and ethylene (ET) signaling to dissect plant responses to diverse 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 oxylipin signaling in mitochondrial stress adaptation. Notably, noxy22/eto1-14, an ET overproducer mutant, displayed broad resistance to all tested inhibitors independently of the canonical mitochondrial retrograde pathway mediated by ANAC017, suggesting a protective role for constitutive ET production. RNA-seq analysis revealed that AA induced ANAC017-regulated genes early and independently of ET signaling, whereas EIN2 was required for later induction of AA-associated defense responses, suggesting that mitochondrial disturbances signal environmental stress through the ET pathway. Accordingly, EIN2 contributed to AA-induced resistance to the biotrophic pathogen Hyaloperonospora arabidopsidis, but not to 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 and immune signaling pathways. Overall design: RNA-seq profiling of 12-day-old wild type (Col0) and ein2-5 plants in response to 20 µM AA 3 h and 24 h after treatment. MS-treated and untreated plants were used as controls.