Two allelic genes responsible for vegetative incompatibility in the fungus Podospora anserina are not essential for cell viability

International audienceVegetative incompatibility is a lethal reaction that destroys the heterokaryotic cells formed by the fusion of hyphae of non-isogenic strains in many fungi. That incompatibility is genetically determined is well known but the function of the genes triggering this rapid cell death is not. The two allelic incompatibility genes, s and S, of the fungus Podospora anserina were characterized. Both encode 30 kDa polypeptides, which differ by 14 amino acids between the two genes. These two proteins are responsible for the incompatibility reaction that results when cells containing s and S genes fuse. Inactivation of the s or S gene by disruption suppresses incompatibility but does not affect the growth or the sexual cycle of the mutant strains. This suggests that these incompatibility genes have no essential function in the life cycle of the fungus

Removing isoflavones from modern soyfood: Why and how?

Estrogenic isoflavones were found, in the 1940s, to disrupt ewe reproduction and were identified in soy-consumers' urine in 1982. This led to controversy about their safety, often supported by current Asian diet measurements, but not by historical data. Traditional Asian recipes of soy were tested while assaying soy glycosilated isoflavones. As these compounds are water-soluble, their concentration is reduced by soaking. Pre-cooking or simmering time-dependently reduces the isoflavone: protein ratio in Tofu. Cooking soy-juice for 15 or 60 min decreases the isoflavone: protein ratios in Tofu from 6.90 to 3.57 and 1.80, respectively (p < 0.001). Traditional Tempeh contains only 18.07% of the original soybean isoflavones (p < 0.001). Soy-juice isoflavones were reduced by ultra-filtration (6.54 vs 1.24 isoflavone: protein; p < 0.001). Soy-protein and isoflavones are dissociated by water rinsing and prolonged cooking, but these have no equivalent in modern processes. As regards human health, a precise definition of the safety level of isoflavone intake requires additional studies. (C) 2016 The Authors. Published by Elsevier Ltd

Identification of surface proteins involved in the adhesion of a probiotic Bacillus cereus strain to mucin and fibronectin

International audienceSeveral Bacillus strains isolated from commercial probiotic preparations were identified at the species level, and their adhesion capabilities to three different model intestinal surfaces (mucin, Matrigel and Caco-2 cells) were assessed. In general, adhesion of spores was higher than that of vegetative cells to the three matrices, and overall strain Bacillus cereusCH displayed the best adhesion. Different biochemical treatments revealed that surface proteins of B. cereusCH were involved in the adhesion properties of the strain. Surface-associated proteins from vegetative cells and spores of B. cereusCH were extracted and identified, and some proteins such as S-layer components, flagellin and cell-bound proteases were found to bind to mucin or fibronectin. These facts suggest that those proteins might play important roles in the interaction of this probiotic Bacillus strain within the human gastrointestinal tract

Biochemical basis for glucose-induced inhibition of malolactic fermentation in Leuconostoc oenos.

The sugar-induced inhibition of malolactic fermentation in cell suspensions of Leuconostoc oenos, recently reclassified as Oenococcus oeni (L. M. T. Dicks, F. Dellaglio, and M. D. Collins, Int. J. Syst. Bacteriol. 45:395-397, 1995) was investigated by in vivo and in vitro nuclear magnetic resonance (NMR) spectroscopy and manometric techniques. At 2 mM, glucose inhibited malolactic fermentation by 50%, and at 5 mM or higher it caused a maximum inhibitory effect of ca. 70%. Galactose, trehalose, maltose, and mannose caused inhibitory effects similar to that observed with glucose, but ribose and 2-deoxyglucose did not affect the rate of malolactic activity. The addition of fructose or citrate completely relieved the glucose-induced inhibition. Glucose was not catabolized by permeabilized cells, and inhibition of malolactic fermentation was not observed under these conditions. 31P NMR analysis of perchloric acid extracts of cells obtained during glucose-malate cometabolism showed high intracellular concentrations of glucose-6-phosphate, 6-phosphogluconate, and glycerol-3-phosphate. Glucose-6-phosphate, 6-phosphogluconate, and NAD(P)H inhibited the malolactic activity in permeabilized cells or cell extracts, whereas NADP+ had no inhibitory effect. The purified malolactic enzyme was strongly inhibited by NADH, whereas all the other above-mentioned metabolites exerted no inhibitory effect, showing that NADH was responsible for the inhibition of malolactic activity in vivo. The concentration of NADH required to inhibit the activity of the malolactic enzyme by 50% was ca. 25 microM. The data provide a coherent biochemical basis to understand the glucose-induced inhibition of malolactic fermentation in L. oenos