Suppression of the SUGAR‐DEPENDENT1 triacylglycerol lipase family during seed development enhances oil yield in oilseed rape (Brassica napus L.)

Increasing the productivity of oilseed crops is an important challenge for plant breeders and biotechnologists. To date, attempts to increase oil production in seeds via metabolic pathway engineering have focused on boosting synthetic capacity. However, in the tissues of many organisms, it is well established that oil levels are determined by both anabolism and catabolism. Indeed, the oil content of rapeseed (Brassica napus L.) has been reported to decline by approximately 10% in the final stage of development, as the seeds desiccate. Here, we show that RNAi suppression of the SUGAR‐DEPENDENT1 triacylglycerol lipase gene family during seed development results in up to an 8% gain in oil yield on either a seed, plant or unit area basis in the greenhouse, with very little adverse impact on seed vigour. Suppression of lipolysis could therefore constitute a new method for enhancing oil yield in oilseed crops.     

Reproductive Biology of the Endemic Fish Etroplus suratensis (Cichlidae) from a Tropical Estuary in Southern India

Journal of Ichthyology - Etroplus suratensis (Bloch, 1790) is a highly exploited endemic cichlid fish species inhabiting the Cochin Estuary situated on the South-west coast of India. The study was...     

Myocardial oxygen consumption change predicts left ventricular relaxation improvement in obese humans after weight loss

Obesity adversely affects myocardial metabolism, efficiency, and diastolic function. Our objective was to determine whether weight loss can ameliorate obesity-related myocardial metabolism and efficiency derangements and that these improvements directly relate to improved diastolic function in humans. We studied 30 obese (BMI >30 kg/m2) subjects with positron emission tomography (PET) (myocardial metabolism, blood flow) and echocardiography (structure, function) before and after marked weight loss from gastric bypass surgery (N = 10) or moderate weight loss from diet (N = 20). Baseline BMI, insulin resistance, hemodynamics, left ventricular (LV) mass, systolic function, myocardial oxygen consumption (MVO2), and fatty acid (FA) metabolism were similar between the groups. MVO2/g decreased after diet-induced weight loss (P = 0.009). Total MVO2 decreased after dietary (P = 0.02) and surgical weight loss (P = 0.0006) and was related to decreased BMI (P = 0.006). Total myocardial FA utilization decreased (P = 0.03), and FA oxidation trended lower (P = 0.06) only after surgery. FA esterification and LV efficiency were unchanged. After surgical weight loss, LV mass decreased by 23% (Doppler-derived) E/E' by 33%, and relaxation increased (improved) by 28%. Improved LV relaxation related significantly to decreased BMI, insulin resistance, total MVO2, and LV mass but not FA utilization. Decreased total MVO(2) predicted LV relaxation improvement independent of BMI change (P = 0.02). Weight loss can ameliorate the obesity-related derangements in myocardial metabolism and LV structure and diastolic function. Decreased total MVO2 independently predicted improved LV relaxation, suggesting that myocardial oxygen metabolism may be mechanistically important in determining cardiac relaxation.     

Signalling mechanisms in the regulation of vacuolar ion release in guard cells

Pharmacological agents were used to investigate the possible involvement of actin in signalling chains associated with abscisic acid (ABA)-induced ion release from the guard cell vacuole, a process which is absolutely essential for stomatal closure. Effects on the ABA-induced transient stimulation of tonoplast efflux were measured, using (86)Rb in isolated guard cells of Commelina communis, together with effects on stomatal apertures. In the response to 10 microm ABA (triggered by Ca(2+) influx rather than internal Ca(2+) release), jasplakinolide (stabilizing actin filaments) and latrunculin B (depolymerizing actin filaments) had opposite effects. Both closure and the vacuolar efflux transient were inhibited by jasplakinolide but enhanced by latrunculin B. At 10 microm ABA prevention of mitogen-activated protein (MAP) kinase activation by PD98059 partially inhibited closure and reduced the efflux transient. By contrast, latrunculin B inhibited the efflux transient at 0.1 microm ABA (involving internal Ca(2+) release rather than Ca(2+) influx). The results suggest that 10 microm ABA activates Ca(2+)-dependent vacuolar ion efflux via a Ca(2+)-permeable influx channel which is maintained closed by interaction with F-actin. A MAP kinase is also involved, in a chain similar to that postulated for Ca(2+)-dependent gene expression in cold acclimation.     

Monocyte-Derived CD11c+ Cells Acquire Plasmodium from Hepatocytes to Prime CD8 T Cell Immunity to Liver-Stage Malaria

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Respiratory fungal allergy

Fungal allergy including allergic rhinitis, conjunctivitis, bronchial asthma, and allergic bronchopulmonary mycoses results from exposure to spores. In this review we have dealt with the common allergenic fungi and allergens, immunopathogenesis, diagnostic assays, and the possible control of allergy in the future based on epitope-specific immunotherapy and vaccination.     

Allosteric interactions and QSAR: on the role of ligand hydrophobicity

A study of a very large database of QSAR (9100) has uncovered a few unusual examples where as one increases the hydrophobicity of the members of a set of congeners, activity decreases until at a certain point, activity begins to increase. Obviously a change in mechanism is involved. The only way we have found to rationalize this unusual event is by a change in the structure of the receptor. We have found this to occur with hemoglobin, a substance first used to define allosteric reactions.     

Searching for allosteric effects via QSARs

A study of our database of 7,000 QSARs involving chemical-biological interaction uncovered 11 examples where the QSARs all contain inverted parabolas based on molecular refractivity. That is, biological activity first decreases with increase in MR and then increases. Two of the examples are for enzymes: cyclooxygenase and trypsin. The others are for various receptors. The results seem to be best rationalized by the larger compounds inducing a change in a receptor unit that allows for a new mode of interaction.     

Photoreceptors for biosynthesis, energy storage and vision

Abstract Living organisms use light as a source of energy and as a means of obtaining information about their environment. Photoreactivating enzyme, provitamins D, retinal (rhodopsins and bacteriorhodopsin), porphyrins (chlorophyll, protochlorophyll and heme), photosynthetic accessory pigments (carotenoids and bilins), phytochrome and riboflavin: these are the molecules which life has settled upon to play the role of light receptor. For some of these photoreceptor molecules a great deal is now known about the chemistry which they perform upon absorbing light; for others virtually nothing is known. Riboflavin, the molecule believed to be functioning in a variety of organisms as the receptor for physiological responses to blue light, is an especially interesting case. Its widespread occurrence in cellular roles other than photoreception make it difficult to separate out the particular flavin which functions as the photoreceptor. It represents a case of a photoreceptor which is at once ubiquitous and elusive.     

Cyclin‐dependent kinase activity enhances phosphatidylcholine biosynthesis in Arabidopsis by repressing phosphatidic acid phosphohydrolase activity

Coordination of endomembrane biogenesis with cell cycle progression is considered to be important in maintaining cell function during growth and development. We previously showed that the disruption of PHOSPHATIDIC ACID PHOSPHOHYDROLASE (PAH) activity in Arabidopsis thaliana stimulates biosynthesis of the major phospholipid phosphatidylcholine (PC) and causes expansion of the endoplasmic reticulum. Here we show that PC biosynthesis is repressed by disruption of the core cell cycle regulator CYCLIN‐DEPENDENT KINASE A;1 (CDKA;1) and that this repression is reliant on PAH. Furthermore, we show that cyclin‐dependent kinases (CDKs) phosphorylate PAH1 at serine 162, which reduces both its activity and membrane association. Expression of a CDK‐insensitive version of PAH1 with a serine 162 to alanine substitution represses PC biosynthesis and also reduces the rate of cell division in early leaf development. Together our findings reveal a physiologically important mechanism that couples the rate of phospholipid biosynthesis and endomembrane biogenesis to cell cycle progression in Arabidopsis.