A microcyst-overproducing mutant of Polysphondylium pallidum

A mutant, PN6017, of the cellular slime mold Polysphondylium pallidum was selected by cell-surface labeling with a monoclonal antibody, mAb 293, and fluorescence-activated cell sorting. The antibody was directed against an L-fucose-containing epitope on glycoproteins, designated ep 293, and the mutant showed reduced and delayed expression of this epitope. PN6017 was distinguished from other mutants of this kind by extensive microcyst formation on agar plates under conditions where the wild type formed only sparse microcysts. In suspension cultures transformation of cells into microcysts was negligible in the wild type, and close to 100% in the mutant. Under these conditions microcyst formation in the mutant began at 5-7 h of starvation. At the same time expression of ep 293 and also of a developmentally regulated cytoplasmic protein, pallidin, became detectable. This coincidence in time suggests that microcyst formation in PN6017 is coupled to the same control mechanism as the two other developmentally regulated processes.     

Macrophage ubiquitin-specific protease 2 modifies insulin sensitivity in obese mice

We previously reported that ubiquitin-specific protease (USP) 2 in macrophages down-regulates genes associated with metabolic diseases, suggesting a putative anti-diabetic role for USP2 in macrophages. In this study, we evaluate this role at both cellular and individual levels. Isolated macrophages forcibly expressing Usp2a, a longer splicing variant of USP2, failed to modulate the insulin sensitivity of 3T3-L1 adipocytes. Similarly, macrophage-selective overexpression of Usp2a in mice (Usp2a transgenic mice) had a negligible effect on insulin sensitivity relative to wild type littermates following a three-month high-fat diet. However, Usp2a transgenic mice exhibited fewer M1 macrophages in their mesenteric adipose tissue. Following a six-month high-fat diet, Usp2a transgenic mice exhibited a retarded progression of insulin resistance in their skeletal muscle and liver, and an improvement in insulin sensitivity at an individual level. Although conditioned media from Usp2a-overexpressing macrophages did not directly affect the insulin sensitivity of C2C12 myotubes compared to media from control macrophages, they did increase the insulin sensitivity of C2C12 cells after subsequent conditioning with 3T3-L1 cells. These results indicate that macrophage USP2A hampers obesity-elicited insulin resistance via an adipocyte-dependent mechanism.     

Preparation of immobilized papain covalently bound on natural cellulose for treatment of beer

Summary Papain was covalently immobilized on both natural wood chip and cotton without substantial loss of enzymic activity, and its optimum pH was 6–10; optimum temperature, 67°C. The immobilized papain showed high activity for hydrolysis of beer peptide and was used in treatment of beer for 28 days without loss of activity.     

Chromate-resistance in a chromate-reducing strain of Enterobacter cloacae

Resistance to toxic hexavalent chromium (chromate: CrO4(2)) in Enterobacter cloacae strain HO1, isolated from an activated sludge sample, was investigated under aerobic and anaerobic conditions. Decreased uptake of 51CrO4(2-) in E. cloacae strain HO1 was observed under aerobic conditions, when compared with a standard laboratory E. cloacae strain (IAM 1624). Under anaerobic conditions E. cloacae strain HO1 was able to reduce hexavalent chromium to the less toxic trivalent form. When E. clocacae strain HO1 was grown with nitrate anaerobically, the cells were observed to lose simultaneously their chromate-reducing ability and chromate-resistance under anaerobic conditions.