The auxin-inducible phosphate transporter AsPT5 mediates phosphate transport and is indispensable for arbuscule formation in Chinese milk vetch at moderately high phosphate supply.

Phosphorus is a macronutrient that is essential for plant survival. Most land plants have evolved the ability to form a mutualistic symbiosis with arbuscular mycorrhizal (AM) fungi, which enhances phosphate (Pi) acquisition. Modulation of Pi transporter systems is the master strategy used by mycorrhizal plants to adapt to ambient Pi concentrations. However, the specific functions of PHOSPHATE TRANSPORTER 1 (PHT1) genes, which are Pi transporters that are responsive to high Pi availability, are largely unknown. Here, we report that AsPT5, an Astragalus sinicus (Chinese milk vetch) member of the PHT1 gene family, is conserved across dicotyledons and is constitutively expressed in a broad range of tissues independently of Pi supply, but is remarkably induced by indole-3-acetic acid (auxin) treatment under moderately high Pi conditions. Subcellular localization experiments indicated that AsPT5 localizes to the plasma membrane of plant cells. Using reverse genetics, we showed that AsPT5 not only mediates Pi transport and remodels root system architecture but is also essential for arbuscule formation in A. sinicus under moderately high Pi concentrations. Overall, our study provides insight into the function of AsPT5 in Pi transport, AM development and the cross-talk between Pi nutrition and auxin signalling in mycorrhizal plants.

Continuous hypothalamic K(ATP) activation blunts glucose counter-regulation in vivo in rats and suppresses K(ATP) conductance in vitro.

AIMS/HYPOTHESIS: Acute systemic delivery of the sulfonylurea receptor (SUR)-1-specific ATP-sensitive K(+) channel (K(ATP)) opener, NN414, has been reported to amplify glucose counter-regulatory responses (CRRs) in rats exposed to hypoglycaemia. Thus, we determined whether continuous NN414 could prevent hypoglycaemia-induced defective counter-regulation. METHODS: Chronically catheterised male Sprague-Dawley rats received a continuous infusion of NN414 into the third ventricle for 8 days after implantation of osmotic minipumps. Counter-regulation was examined by hyperinsulinaemic-hypoglycaemic clamp on day 8 after three episodes of insulin-induced hypoglycaemia (recurrent hypoglycaemia [RH]) on days 5, 6 and 7. In a subset of rats exposed to RH, NN414 infusion was terminated on day 7 to wash out NN414 before examination of counter-regulation on day 8. To determine whether continuous NN414 exposure altered K(ATP) function, we used the hypothalamic glucose-sensing GT1-7 cell line, which expresses the SUR-1-containing K(ATP) channel. RESULTS: Continuous exposure to NN414 in the setting of RH increased, rather than decreased, the glucose infusion rate (GIR), as exemplified by attenuated adrenaline (epinephrine) secretion. Termination of NN414 on day 7 with subsequent washout for 24 h partially diminished the GIR. The same duration of exposure of GT1-7 cells to NN414 substantially reduced K(ATP) conductance, which was also reversed on washout of the agonist. The suppression of K(ATP) current was not associated with reduced channel subunit mRNA or protein levels. CONCLUSIONS/INTERPRETATION: These data indicate that continuous K(ATP) activation results in suppressed CRRs to hypoglycaemia in vivo, which in vitro is associated with the reversible conversion of KATP into a stable inactive state.

Rhamnolipids enhance marine oil spill bioremediation in laboratory system.

This paper presents a simulated marine oil spill bioremediation experiment using a bacterial consortium amended with rhamnolipids. The role of rhamnolipids in enhancing hydrocarbon biodegradation was evaluated via GC-FID and GC-MS analysis. Rhamnolipids enhanced total oil biodegradation efficiency by 5.63%, with variation in normal alkanes, polyaromatic hydrocarbons (PAHs) and biomakers biodegradation. The hydrocarbons biodegradation by bacteria consortium overall follows a decreasing order of PAHs>n-alkanes>biomarkers, while in different order of PAHs>biomarkers>n-alkanes when rhamnolipids was used, and the improvement in the removal efficiency by rhamnolipids follows another order of biomarkers>n-alkanes>PAHs. Rhamnolipids played a negative role in degradation of those hydrocarbons with relatively volatile property, such as n-alkanes with short chains, PAHs and sesquiterpenes with simple structure. As to the long chain normal alkanes and PAHs and biomakers with complex structure, the biosurfactant played a positive role in these hydrocarbons biodegradation.

Hypothalamic Fkbp51 is induced by fasting, and elevated hypothalamic expression promotes obese phenotypes.

To discover hypothalamic genes that might play a role in regulating energy balance, we carried out a microarray screen for genes induced by a 48-h fast in male C57Bl/6J mouse hypothalamus. One such gene was Fkbp51 (FK506 binding protein 5; Locus NP_034350). The product of this gene is of interest because it blocks glucocorticoid action, suggesting that fasting-induced elevation of this gene in the hypothalamus may reduce glucocorticoid negative feedback, leading to elevated glucocorticoid levels, thus promoting obese phenotypes. Subsequent analysis demonstrated that a 48-h fast induces Fkbp51 in ventromedial, paraventricular, and arcuate hypothalamic nuclei of mice and rats. To assess if hypothalamic Fkbp51 promotes obesity, the gene was transferred to the hypothalamus via an adeno-associated virus vector. Within 2 wk following Fkbp51 overexpression, mice on a high-fat diet exhibited elevated body weight, without hyperphagia, relative to mice receiving the control mCherry vector. Body weight remained elevated for more than 8 wk and was associated with elevated corticosterone and impaired glucose tolerance. These studies suggest that elevated hypothalamic Fkbp51 promotes obese phenotypes.

Radix astragali (huangqi) as a treatment for defective hypoglycemia counterregulation in diabetes.

Radix astragali is a herbal remedy used in China to treat patients with diabetes exposed to repeated episodes of hypoglycemia. The physiological basis or validity of this approach is not clear. In the present study, we examine the effect of pre-treatment with Radix astragali on hormonal counterregulatory responses to hypoglycemia in normal male Sprague-Dawley rats. Four groups of rodents were studied. In two of these groups, rodents were pre-treated for 3 days with either intravenous Radix astragali or control solution and, subsequently, while awake and unrestrained, underwent an in vivo hyperinsulinemic hypoglycemic (50 mg/dl) clamp study. The rodents in other two groups were pre-treated for 7 days with either intravenous Radix astragali or control solution. In addition, for the last 3-days of their treatment, the rats were subjected to a once-daily episode of insulin-induced hypoglycemia. Upon completion of this protocol, each rat underwent a controlled in vivo hyperinsulinemic hypoglycemic (50 mg/dl) clamp study. Radix astragali was shown to amplify the glucose counterregulatory response to hypoglycemia in both untreated and recurrently hypoglycemic rats. Immunocytochemistry studies suggested this might reflect increased neural activation in two key central glucose-sensing regions, the paraventricular hypothalamus and the nucleus tractus solitarius. Based on these rodent studies, we conclude that Radix astragali pre-treatment can amplify the counterregulatory response to hypoglycemia through a mechanism that may involve the central glucose-sensing regions. Future studies to examine the potential therapeutic benefit of Radix astragali in rodent models of type 1 diabetes are warranted.