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Abstract
Mitochondrial uncoupling protein 1 (UCP1) decreases reactive oxygen species production under stress conditions by uncoupling the electrochemical gradient from ATP synthesis. This study combined transcriptome profiling with experimentally induced hypoxia to mechanistically dissect the impact of Arabidopsis thaliana UCP1 (AtUCP1) overexpression in tobacco. Transcriptomic analysis of AtUCP1-overexpressing (P07) and wild-type (WT) plants was carried out using RNA sequencing. Metabolite and carbohydrate profiling of hypoxia-treated plants was performed using (1)H-nuclear magnetic resonance spectroscopy and high-performance anion-exchange chromatography with pulsed amperometric detection. The transcriptome of P07 plants revealed a broad induction of stress-responsive genes that were not strictly related to the mitochondrial antioxidant machinery, suggesting that overexpression of AtUCP1 imposes a strong stress response within the cell. In addition, transcripts that mapped into carbon fixation and energy expenditure pathways were broadly altered. It was found that metabolite markers of hypoxic adaptation, such as alanine and tricarboxylic acid intermediates, accumulated in P07 plants under control conditions at similar rates to WT plants under hypoxia. These findings indicate that constitutive overexpression of AtUCP1 induces a hypoxic response. The metabolites that accumulated in P07 plants are believed to be important in signalling for an improvement in carbon assimilation and induction of a hypoxic response. Under these conditions, mitochondrial ATP production is less necessary and fermentative glycolysis becomes critical to meet cell energy demands. In this scenario, the more flexible energy metabolism along with an intrinsically activated hypoxic response make these plants better adapted to face several biotic and abiotic stresses.
Highlights
Mitochondrial uncoupling proteins (UCPs) comprise a fam- 2006)
These findings indicate that constitutive overexpression of Arabidopsis thaliana UCP1 (AtUCP1) induces a hypoxic response
Transcripts that mapped into the pathways related to energy expenditure, which included ‘sugar degradation’, ‘glycolysis’, ‘fermentation’, ‘oxidative pentose phosphate’, ‘tricarboxylic acid cycle (TCA)’, and ‘mitochondrial electron transport chain’, were mostly upregulated
Summary
Mitochondrial uncoupling proteins (UCPs) comprise a fam- 2006). the biochemical mechanisms and relevance ily of nuclear-encoded proteins that are localized to the mito- of UCPs are not completely understood, it is known that its chondrial inner membrane (Krauss et al, 2005; Vercesi et al, activation results in the re-entry of H+ from the intermembrane302 | Barreto et al.space back into the mitochondrial matrix, reducing oxidative phosphorylation (OXPHOS) efficiency (Figueira et al, 2013). The phenotype of plants overexpressing UCPs have been explained in terms of decreased ROS production by the mitochondrial electron transport chain (Brandalise et al, 2003; Begcy et al, 2011; Chen et al, 2013), which benefits adaptation of the plant to biotic and abiotic stresses and the plant’s capacity to assimilate carbon under control conditions
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