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. 2020 Oct 27;223(20):jeb227801. doi: 10.1242/jeb.227801

Fig. 1.

Fig. 1. Many mitochondrial processes can be affected by temperature. Most studies on the effects of temperature on mitochondria have focused on the ability of these organelles to generate ATP through oxidative phosphorylation. The first step in this process is substrate transport (A) into the mitochondria, followed by substrate oxidation (B) by the tricarboxylic acid cycle (TCA cycle) to generate the electron carriers nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FADH2). These carriers donate their electrons to the proteins of the electron transport system (ETS) (C) in the inner mitochondrial membrane (IMM). The ETS performs a series of redox reactions and harnesses the resulting free energy to drive proton transport (through ETS complexes I, III and IV) from the matrix to the inter-membrane space to generate the proton motive force (PMF) (D). The energy stored in the PMF is then utilized by the F1FO-ATP synthase, also known as complex V of the oxidative phosphorylation system, in the process of ATP synthesis (E), and the resulting ATP is exported from the mitochondria via the adenine nucleotide translocator (ANT). Inefficiencies can arise owing to the loss of PMF via proton leak (F), which can occur via several pathways including directly through the IMM or via proteins such as the ANT and uncoupling proteins (UCP), decreasing the driving force to synthesize ATP. These functions occur in the context of the lipid environment of the IMM, which itself can vary among species or with thermal acclimation, with potential effects on mitochondrial performance. Mitochondrial function generates free radicals (e.g. reactive oxygen species; ROS). The balance between ROS production and detoxification (G) is critical because ROS act as important intracellular signaling molecules at low concentrations but become damaging as their production exceeds mitochondrial and cellular detoxification capacity. Mitochondrial structure (H), which is critical for function, is also dynamic and can be altered through processes including fission and fusion, which may be affected by temperature. Under extreme cellular stress, a protein complex called the permeability transition pore (PTP) (I) can form, causing the release of cytochrome c, triggering cellular apoptosis or necrosis. There is also strong evidence of a relationship between variation in the mitochondrial genome (J) and whole-organism thermal tolerance, emphasizing the potential importance of mitochondrial processes in determining organismal thermal limits. Succ, succinate; Fum, fumarate.

Many mitochondrial processes can be affected by temperature. Most studies on the effects of temperature on mitochondria have focused on the ability of these organelles to generate ATP through oxidative phosphorylation. The first step in this process is substrate transport (A) into the mitochondria, followed by substrate oxidation (B) by the tricarboxylic acid cycle (TCA cycle) to generate the electron carriers nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FADH2). These carriers donate their electrons to the proteins of the electron transport system (ETS) (C) in the inner mitochondrial membrane (IMM). The ETS performs a series of redox reactions and harnesses the resulting free energy to drive proton transport (through ETS complexes I, III and IV) from the matrix to the inter-membrane space to generate the proton motive force (PMF) (D). The energy stored in the PMF is then utilized by the F1FO-ATP synthase, also known as complex V of the oxidative phosphorylation system, in the process of ATP synthesis (E), and the resulting ATP is exported from the mitochondria via the adenine nucleotide translocator (ANT). Inefficiencies can arise owing to the loss of PMF via proton leak (F), which can occur via several pathways including directly through the IMM or via proteins such as the ANT and uncoupling proteins (UCP), decreasing the driving force to synthesize ATP. These functions occur in the context of the lipid environment of the IMM, which itself can vary among species or with thermal acclimation, with potential effects on mitochondrial performance. Mitochondrial function generates free radicals (e.g. reactive oxygen species; ROS). The balance between ROS production and detoxification (G) is critical because ROS act as important intracellular signaling molecules at low concentrations but become damaging as their production exceeds mitochondrial and cellular detoxification capacity. Mitochondrial structure (H), which is critical for function, is also dynamic and can be altered through processes including fission and fusion, which may be affected by temperature. Under extreme cellular stress, a protein complex called the permeability transition pore (PTP) (I) can form, causing the release of cytochrome c, triggering cellular apoptosis or necrosis. There is also strong evidence of a relationship between variation in the mitochondrial genome (J) and whole-organism thermal tolerance, emphasizing the potential importance of mitochondrial processes in determining organismal thermal limits. Succ, succinate; Fum, fumarate.