Oxidative respiration produces adenosine triphosphate through the mitochondrial electron transport system controlling the energy supply of plant cells. Here we describe a mitochondrial pentatricopeptide repeat (PPR) domain protein, PPR40, which provides a signaling link between mitochondrial electron transport and regulation of stress and hormonal responses in Arabidopsis (Arabidopsis thaliana). Insertion mutations inactivating PPR40 result in semidwarf growth habit and enhanced sensitivity to salt, abscisic acid, and oxidative stress. Genetic complementation by overexpression of PPR40 complementary DNA restores the ppr40 mutant phenotype to wild type. The PPR40 protein is localized in the mitochondria and found in association with Complex III of the electron transport system. In the ppr40-1 mutant the electron transport through Complex III is strongly reduced, whereas Complex IV is functional, indicating that PPR40 is important for the ubiqinol-cytochrome c oxidoreductase activity of Complex III. Enhanced stress sensitivity of the ppr40-1 mutant is accompanied by accumulation of reactive oxygen species, enhanced lipid peroxidation, higher superoxide dismutase activity, and altered activation of several stress-responsive genes including the alternative oxidase AOX1d. These results suggest a close link between regulation of oxidative respiration and environmental adaptation in Arabidopsis.Adaptation of plants to environmental stresses has important metabolic implications, including changes in photosynthesis, respiration, metabolite assimilation, and catabolism. Mitochondria are in the center of regulation of cellular energy homeostasis and redox balance, and integrate numerous metabolic pathways that are important in adaptive responses to extreme environmental conditions. Respiration and oxidative phosphorylation; metabolism of Pro, Cys, ascorbate, and folate; and the control of redox balance are examples of processes illustrating the importance of mitochondria in coordination of cellular metabolism during stress adaptation (Sweetlove et al., 2007).Respiration is the core process of mitochondrial metabolism in which a large amount of free energy is released and used for ATP production. During respiration, controlled oxidation of reduced carbohydrates, such as malate and pyruvate, takes place through glycolysis and tricarboxylic acid cycle producing, respectively, reducing NADPH and FADH 2 . Electrons from the NADPH and FADH 2 are transferred to O 2 via the electron transport chain generating the energy carrier ATP and oxidized NADP 1 and FAD

Auxin and cytokinin are key endogenous regulators of plant development. Although cytokinin-mediated modulation of auxin distribution is a developmentally crucial hormonal interaction, its molecular basis is largely unknown. Here we show a direct regulatory link between cytokinin signalling and the auxin transport machinery uncovering a mechanistic framework for cytokinin-auxin cross-talk. We show that the CYTOKININ RESPONSE FACTORS (CRFs), transcription factors downstream of cytokinin perception, transcriptionally control genes encoding PIN-FORMED (PIN) auxin transporters at a specific PIN CYTOKININ RESPONSE ELEMENT (PCRE) domain. Removal of this cis-regulatory element effectively uncouples PIN transcription from the CRF-mediated cytokinin regulation and attenuates plant cytokinin sensitivity. We propose that CRFs represent a missing cross-talk component that fine-tunes auxin transport capacity downstream of cytokinin signalling to control plant development.