No abstract

Increased aerobic glycolysis in endothelial cells of atheroprone areas of blood vessels has been hypothesized to drive increased inflammation and lesion burden but direct links remain to be established. Here we show that endothelial cells exposed to disturbed flow in vivo and in vitro exhibit increased levels of protein kinase AMP-activated (PRKA)/AMP-activated protein kinases (AMPKs). Selective deletion of endothelial Prkaa1, coding for protein kinase AMP-activated catalytic subunit alpha1, reduces glycolysis, compromises endothelial cell proliferation, and accelerates the formation of atherosclerotic lesions in hyperlipidemic mice. Rescue of the impaired glycolysis in Prkaa1-deficient endothelial cells through Slc2a1 overexpression enhances endothelial cell viability and integrity of the endothelial cell barrier, and reverses susceptibility to atherosclerosis. In human endothelial cells, PRKAA1 is upregulated by disturbed flow, and silencing PRKAA1 reduces glycolysis and endothelial viability. Collectively, these results suggest that increased glycolysis in the endothelium of atheroprone arteries is a protective mechanism.

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Understanding how agricultural management practices impact nitrous oxide (N 2 O) emissions is prerequisite for developing mitigation protocols. We conducted a meta-analysis on 597 pairwise comparisons (129 papers) to assess how management affects N 2 O emissions. Pairwise comparisons of practices aimed at improving fertilizer use efficiency (39%) and tillage (30%) dominated the dataset, while ecologically-based nutrient management (ENM) practices constituted 15% of the pairs. In general, across management practices, the quantity of N added was a more significant driver of N 2 O fluxes than was the form of N (fertilizer, legume biomass or animal manures). Manure interacted with soil texture so that in coarse soils, N 2 O emissions from manures tended to be higher compared to inorganic N fertilizers. The studies of ENM strategies frequently involved overapplication of N inputs in the ENM treatments. Cover crops reduced N 2 O emissions compared to bare fallows. However, during the cash crop growing season, when differences in N added and N source were confounded, the extra N inputs from cover crops were significantly correlated with the differences in N 2 O emissions between treatments with and without cover crops. Overall, in 38% of the data pairs, N 2 O emissions were reduced with limited impacts on yields; in half of these pairs, yields were maintained or increased while in the other half they were reduced by only B10%. Knowledge gaps on mitigation of agricultural N 2 O emissions could be addressed by applying an ecosystem-based, cross-scale perspective in conjunction with the N saturation conceptual framework to guide research priorities and experimental designs.

Iron is a critical cofactor for a number of metalloenzymes involved in respiration and photosynthesis, but plants often suffer from iron deficiency due to limited supplies of soluble iron in the soil. Iron deficiency induces a series of adaptive responses in various plant species, but the mechanisms by which they are triggered remain largely unknown. Using pH imaging and hormone localization techniques, it has been demonstrated here that root Fe(III) reductase activity and proton extrusion upon iron deficiency are up-regulated by systemic auxin signalling in a Fe-efficient woody plant, Malus xiaojinensis. Split-root experiments demonstrated that Fe-deprivation in a portion of the root system induced a dramatic increase in Fe(III) reductase activity and proton extrusion in the Fe-supplied portion, suggesting that the iron deficiency responses were mediated by a systemic signalling. Reciprocal grafting experiments of M. xiaojinensis with Malus baccata, a plant with no capability to produce the corresponding responses, indicate that the initiation of the systemic signalling is likely to be determined by roots rather than shoots. Iron deficiency induced a substantial increase in the IAA content in the shoot apex and supplying exogenous IAA analogues (NAA) to the shoot apex could mimic the iron deficiency to trigger the corresponding responses. Conversely, preventing IAA transport from shoot to roots blocked the iron deficiency responses. These results strongly indicate that the iron deficiency-induced physiological responses are mediated by systemic auxin signalling.