Plant respiration: Controlled by photosynthesis or biomass?

Two simplifying hypotheses have been proposed for whole‐plant respiration. One links respiration to photosynthesis; the other to biomass. Using a first‐principles carbon balance model with a prescribed live woody biomass turnover, applied at a forest research site where multidecadal measurements are available for comparison, we show that if turnover is fast the accumulation of respiring biomass is low and respiration depends primarily on photosynthesis; while if turnover is slow the accumulation of respiring biomass is high and respiration depends primarily on biomass. But the first scenario is inconsistent with evidence for substantial carry‐over of fixed carbon between years, while the second implies far too great an increase in respiration during stand development—leading to depleted carbohydrate reserves and an unrealistically high mortality risk. These two mutually incompatible hypotheses are thus both incorrect. Respiration is not linearly related either to photosynthesis or to biomass, but it is more strongly controlled by recent photosynthates (and reserve availability) than by total biomass.     

Does elevated atmospheric CO2 concentration inhibit mitochondrial respiration in green plants?

ATP, adenosine triphosphate
K_m, Michaelis-Menton coefficient
C_a, concentration of CO₂ in the air (μmol mol^–1)
NAD, oxidized nicotin adenine dinucleotide
NADH, reduced nicotin adenine dinucleotide
NADP, oxidized nicotin adenine phosphate dinucleotide
NADPH, reduced nicotine adenine phosphate dinucleotide
R, rate of respiration per unit DW [μmol g
DW^–1], Rubisco, ribulose-1,5-bisphosphate carboxylase/oxygenase
V_c,_max, maximum in vivo rate of carboxylation at Rubisco (μmol m^–2 s^–1)

There is abundant evidence that a reduction in mitochondrial respiration of plants occurs when atmospheric CO₂ (C_a) is increased. Recent reviews suggest that doubling the present C_a will reduce the respiration rate [per unit dry weight (DW)] by 15 to 18%. The effect has two components: an immediate, reversible effect observed in leaves, stems, and roots of plants as well as soil microbes, and an irreversible effect which occurs as a consequence of growth in elevated C_a and appears to be specific to C₃ species. The direct effect has been correlated with inhibition of certain respiratory enzymes, namely cytochrome-c-oxidase and succinate dehydrogenase, and the indirect or acclimation effect may be related to changes in tissue composition. Although no satisfactory mechanisms to explain these effects have been demonstrated, plausible mechanisms have been proposed and await experimental testing. These are carbamylation of proteins and direct inhibition of enzymes of respiration. A reduction of foliar respiration of 15% by doubling present ambient C_a would represent 3 Gt of carbon per annum in the global carbon budget.     

Bcl-2 proteins: regulators of apoptosis or of mitochondrial homeostasis?

Programmed cell death (apoptosis) is used by multicellular organisms during development and to maintain homeostasis within mature tissues. One of the first genes shown to regulate apoptosis was bcl-2. Subsequently, a number of Bcl-2-related proteins have been identified. Despite overwhelming evidence that Bcl-2 proteins are evolutionarily conserved regulators of apoptosis, their precise biochemical function remains controversial. Three biochemical properties of Bcl-2 proteins have been identified: their ability to localize constitutively and/or inducibly to the outer mitochondrial, outer nuclear and endoplasmic reticular membranes, their ability to form heterodimers with proteins bearing an amphipathic helical BH3 domain, and their ability to form ion-conducting channels in synthetic membranes. The discovery that mitochondria can play a key part in the induction of apoptosis has focused attention on the role that Bcl-2 proteins may have in regulating either mitochondrial physiology or mitochondria-dependent caspase activation. Here we attempt to synthesize our current understanding of the part played by mitochondria in apoptosis with a consideration of how Bcl-2 proteins might control cell death through an ability to regulate mitochondrial physiology.     

Can stomatal closure caused by xylem ABA explain the inhibition of leaf photosynthesis under soil drying?

Effects of leaf water deficit and increase in endogenous ABA on photosynthesis of two tropical trees, t Acacia confusa and t Leucaena leucocephala, were investigated with two soil-drying methods, i.e. half or whole root system was subjected to soil drying. Half-root drying was achieved by allowing upper layer of soil column to dry and lower layer of soil column to remain watered. Half-root drying had little effect on leaf water potential, but when compared to the well-watered control, both methods of soil drying substantially increased the ABA concentration in xylem and reduced leaf conductance in both species. There was a significant relationship between leaf conductance and xylem ABA concentrations in both species, which was comparable to the same relationship that was generated by feeding ABA to excised twigs. The rate of photosynthesis was inhibited substantially in both soil-drying treatments and in both species, but photochchemical efficiency, measured as a ratio of variable fluorescence to a peak fluorescence emission of a dark-adapted leaf (F_v/F_m), was not reduced except in the whole root-dried t L. leucocephala plants where leaf water potential was reduced to –2.5 MPa. In all the cases where photosynthesis was inhibited, there was a concomitant reduction in both leaf conductance and calculated internal CO₂ concentration. After two days of rewatering, leaf water potential and xylem ABA concentration rapidly returned to pre-treatment levels, but leaf conductance and photosynthesis of both whole-root and half root dried t L. leucocephala remained inhibited substantially. Rewatering led to a full recovery of both stomatal conductance and photosynthesis in soil-dried t A. confusa, although its photosynthesis of whole-root dried plants did not recover fully but such difference was not significant statistically. These results suggest that drought-induced decline of photosynthesis was mainly a result of the stomatal factor caused by the increase of ABA concentration in the xylem sap. Non-stomatal factors, e.g. reduced photochemical activity and/or carbon metabolic activity, were species-specific and were brought about only at very low water potential.     

The mitochondrial theory of aging: dead or alive?

The mitochondrial theory of aging is based around the idea of a vicious cycle, in which somatic mutation of mtDNA engenders respiratory chain dysfunction, enhancing the production of DNA-damaging oxygen radicals. In turn, this is proposed to result in the accumulation of further mtDNA mutations. Finally, a bioenergetic crisis leads to overt tissue dysfunction and degeneration. A substantial body of circumstantial evidence seems to support this idea. However, the extent of detectable mtDNA mutation is far less than can easily be reconciled to this hypothesis, unless it is assumed that a subset of cells with much higher than average mtDNA mutation load is systematically lost by apoptosis. A rigorous test of the hypothesis remains to be undertaken, but would require a direct manipulation of the rate of mtDNA mutagenesis, to test whether this could alter the kinetics of aging.     

Colicin E2 release: lysis,leakage or secretion? Possible role of a phospholipase.

Results presented here and by others indicate that the release of colicins from producing cells can be uncoupled from the decline in culture turbidity which usually occurs within 2-3 h after the induction of colicin synthesis. This excludes lysis as a necessary event in colicin release. Conversely, the failure to dissociate colicin release from the normally simultaneous release of a specific subset of soluble proteins argues against the idea of a specific colicin secretion system sensu-stricto. Rather, colicin release appears to be a consequence of semi-specific leakage resulting from an alteration of the permeability properties of the cell envelope. This alteration is caused by the 'lysis protein' known to be encoded by most multiple copy number Col plasmids. The finding that the expression of the lysis gene of plasmid ColE2 renders the cells exquisitely sensitive to lysozyme demonstrates that the permeability of the outer membrane must indeed be altered. Evidence is presented that this alteration could be due at least in part to the activation of the detergent-resistant phospholipase A (pldA product). Lysophosphatidylethanolamine, a product of the action of phospholipase on phosphatidylethanolamine, is a membrane perturbant which could alter the permeability properties of the envelope and allow some proteins such as colicin to leak out of the cell.     

The inheritance of mitochondrial DNA heteroplasmy: random drift, selection or both?

The mammalian mitochondrial genome (mtDNA) is a small double-stranded DNA molecule that is exclusively transmitted down the maternal line. Pathogenic mtDNA mutations are usually heteroplasmic, with a mixture of mutant and wild-type mtDNA within the same organism. A woman harbouring one of these mutations transmits a variable amount of mutant mtDNA to each offspring. This can result in a healthy child or an infant with a devastating and fatal neurological disorder. Understanding the biological basis of this uncertainty is one of the principal challenges facing scientists and clinicians in the field of mitochondrial genetics.     

A re-interpretation of lipoxygenase-dependent insulin release: which metabolites of arachidonic acid, or none?

There are considerable data implicating a pancreatic islet 12-lipoxy-genase in glucose-induced insulin secretion. This enzyme traditionally is conceived as converting unesterified arachidonic acid to "free" hydroperoxyeicosatetraenoic acid and metabolites thereof. However, studies employing the provision of exogenous metabolites of arachidonic acid to islet tissue fail to identify convincingly the mediator of insulin release. It is proposed that the islet lipoxygenase directly peroxidizes unsaturated fatty acids esterified within membrane phospholipids, leading to changes in ion flux and enzyme activity (particularly phospholipase A2) at the membrane level. The release of unesterified metabolites of arachidonate, although reflecting islet lipoxygenase activity, may be an epiphenomenon.     

Soil respiration under prolonged soil warming: are rate reductions caused by acclimation or substrate loss?

The world's soils contain a large amount of carbon so that even a fractionally small loss or gain could have a quantitatively important feedback effect on net CO₂ emissions to the atmosphere. It is therefore important to fully understand the temperature dependence of soil‐carbon decomposition. Evidence from various observations can be used to quantify the temperature dependence of carbon efflux, but it is important to ensure that confounding factors, such as changing water relations or availability of readily decomposable substrate, are fully considered in inferring an underlying temperature response from observed response patterns. A number of recent findings from soil‐warming experiments have led to the suggestion that stimulation of soil‐carbon efflux by increasing temperature is only transitory before acclimation takes place and carbon efflux rates return to similar rates as before the increase in temperature. It is shown here that this response pattern can be explained through a simple two‐pool soil‐carbon model with no acclimation response needing to be invoked. The temporal pattern is, instead, due to depletion of readily decomposable substrate. It shows that findings of reduced respiration rate in soil‐warming experiments are consistent with unchanged high temperature sensitivity of organic carbon decomposition and affirms that there is, indeed, a danger of positive feedback between global warming and the release of soil organic carbon that can lead to further warming.     

Stimulation of ACTH release by naloxone: Central or peripheral action?

The concentration of ACTH and corticosterone in plasma were measured following peripheral administration of naloxone and naloxone methylbromide (quaternary derivative of opiate antagonist naloxone which is thought not to cross the blood brain barrier) in male rats. Subcutaneous administration of naloxone methylbromide in the dose range of 0.625 - 5.0 mg kg-1 resulted in a small but significant increase in plasma corticosterone levels. Both naloxone and its quaternary derivative injected via permanent intraperitoneal catheters to freely moving rats induced a highly significant increase in plasma ACTH levels measured in blood obtained via permanent tail artery catheters 30 min following injection. These results indicate that loci outside the blood brain barrier are, at least partially, involved in the naloxone-induced stimulation of ACTH release.     

Excitation,inhibition, local oscillations,or large-scale loops: what causes the symptoms of schizophrenia?

What causes the positive, negative, and cognitive symptoms of schizophrenia? The importance of circuits is underscored by the finding that no single gene contributes strongly to the disease. Thus, some circuit abnormality to which many proteins can contribute is the likely cause. There are several major hypotheses regarding the circuitry involved: first, a change in the balance of excitation/inhibition in the prefrontal cortex (PFC); second, abnormal EEG oscillations in the gamma range; third, an increase in theta/delta EEG power related to changes in the thalamus (particularly midline nuclei); fourth, hyperactivity in the hippocampus and consequent dopamine hyperfunction; and fifth, deficits in corollary discharge. Evidence for these hypotheses will be reviewed.     

Putative partners in Bax mediated cytochrome-c release: ANT,CypD, VDAC or none of them?

Release of cytochrome-c from mitochondria is a key regulatory event in the intrinsic pathway of apoptosis, and its mechanism has been the subject of extensive debate with investigators proposing different and contrasting models. While some models suggest that cytochrome-c release can occur in absence of permeability transition and is mediated by the pro-apoptotic protein Bax, some suggest involvement of various components of permeability transition pore with or without cooperative action of Bax. Various models of PTP-dependent or -independent cytochrome-c release are discussed in this review with special emphasis on all the independent/cooperative roles of Bax evidenced so far.     

Prostaglandin-mediated inhibition of noradrenaline release: V. A comparison of the neuroinhibitory effect of three prostaglandins: E2, I2, and 6-keto-PGF1α

The effect of PGE₂, PGI₂, and 6-keto-PGF_1α respectively on the contractile response of the isolate , field-stimulated guinea pig vas deferens was investigated. All three PGs were capable of inhibiting the contractile responses of the vas deferens, but the concentrations required varied considerably: PGE₂ was about 700 times more active than PGI₂ and about 4600 times more active than 6-keto-PGF_1α in this respect. It is suggested that PGI₂, although formed in tissues with sympathetic innervation, does not play a physiological role as inhibitor of sympathetic transmitter release.     

Fatty acids revert the inhibition of respiration caused by the antidiabetic drug metformin to facilitate their mitochondrial β-oxidation

While metformin has been widely used to treat type 2 diabetes for the last fifty years, its mode of action remains unclear. Hence, we investigated the short-term alterations in energy metabolism caused by metformin administration in 3T3-L1 adipocytes. We found that metformin inhibited mitochondrial respiration, although ATP levels remained constant as the decrease in mitochondrial production was compensated by an increase in glycolysis. While AMP/ATP ratios were unaffected by metformin, phosphorylation of AMPK and its downstream target acetyl-CoA carboxylase augmented. The inhibition of respiration provoked a rapid and sustained increase in superoxide levels, despite the increase in UCP2 and superoxide dismutase activity. The inhibition of respiration was rapidly reversed by fatty acids and thus respiration was lower in treated cells in the presence of pyruvate and glucose while rates were identical to control cells when palmitate was the substrate. We conclude that metformin reversibly inhibits mitochondrial respiration, it rapidly activates AMPK without altering the energy charge, and it inhibits fatty acid synthesis. Mitochondrial β-oxidation is facilitated by reversing the inhibition of complex I and, presumably, by releasing the inhibition of carnitine palmitoyltransferase. This article is part of a Special Issue entitled: 17th European Bioenergetics Conference (EBEC 2012).