Extracellular suppression allows mating by pheromone-deficient sterile mutants of Saccharomyces cerevisiae

MAT alpha haploids with mutations in the STE13 or KEX2 gene, and MATa haploids with mutations in the STE6 or STE14 gene, do not mate with wild-type cells of the opposite mating type. We found that such mutants were able to mate with partners that carry mutations (sst1 and sst2) that cause cells to be supersensitive to yeast mating pheromone action. Mating ability of MAT alpha ste13 and MAT alpha kex2 mutants could also be restored by adding normal MAT alpha cells to mating mixtures or by adding just the appropriate purified pheromone (alpha-factor). Therefore, the mating deficiencies caused by the ste13 and kex2 lesions, and by inference, the ste6 and ste14 mutations, appear to result only from secretion of an insufficient amount of pheromone or a nonfunctional pheromone.     

Metabolism of caffeine by mouse liver microsomes: GSH or cytosol causes a shift in products from 1, 3, 7-trimethylurate to a substituted diaminouracil

Incubation of [¹⁴C] caffeine with hepatic microsomes from male AKR/J mice resulted in the formation of several metabolites including 1, 3, 7-trimethylurate and 6-amino-5-(N-formylmethyl-amino)-1, 3-dimethyluracil. These two compounds comprised about 60% of products and are major urinary metabolites in several animals. When cytosol was included during incubation, there was a 14-fold increase in yield of the uracil at the expense of the urate; the combination of the two metabolites remained about 60% of total products. Cytosol alone was catalytically inert. Glutathione and other sulfhydryl compounds reproduced the effect of cytosol, and the action of cytosol was accounted for quantitatively by its sulfhydryl content. We propose that an oxidized intermediate of caffeine en route to trimethylurate is reduced by glutathione to the ring-opened uracil derivative.     

Functional Effects of Adiponectin on Endothelial Progenitor Cells

Adiponectin is an adipokine whose plasma levels are inversely correlated to metabolic syndrome components. Adiponectin protects against atherosclerosis and decreases risks in myocardial infarction. Endothelial progenitor cells (EPCs) are a heterogeneous population of circulating cells involved in vascular repair and neovascularization. EPCs number is reduced in patients with cardiovascular disease. We hypothesize that the positive effects of adiponectin against atherosclerosis are explained in part by its interactions with EPCs. Cells were obtained from healthy volunteers' blood by mononuclear cell isolation and plating on collagen‐coated dishes. Three sub‐populations of EPCs were identified and characterized using flow cytometry. EPCs' expression of adiponectin receptors, AdipoR1, and AdipoR2 was evaluated by quantitative PCR. The effects of recombinant adiponectin on EPCs' susceptibility to apoptosis were assessed. Finally, expression of neutrophil elastase by EPCs and activity of this enzyme on adiponectin processing were assessed. Quantitative PCR analysis of EPCs mRNAs showed that AdipoR1 mRNA is expressed at higher levels than AdipoR2. Expression of AdipoR1 protein was confirmed by western blot. Adiponectin significantly increased survival of two sub‐populations of EPCs in conditions of serum deprivation. Such effect could not be demonstrated in the third EPCs sub‐population. We also demonstrated that EPCs, particularly one sub‐population, express neutrophil elastase. Neutrophil elastase activity was confirmed in EPCs' conditioned media. Adiponectin protects some EPCs sub‐populations against apoptosis and therefore could modulate EPCs ability to induce repair of vascular damage. Neutrophil elastase activity of EPCs could locally modulate adiponectin activity by its involvement in the generation of the globular form of adiponectin.     

Prostaglandin-sepharose: Application to the purification of bovine lung 15 (S) -hydroxyprostaglandin dehydrogenase

Prostaglandins E₁, F_1α and A₂ were covalently joined to the surface of Sepharose as carboxamide linkages. The insolubilized prostaglandins were shown to function effectively in the purification of 15(S) -hydroxyprostaglandin dehydrogenase.     

When Landscaping Goes Bad: The Incipient Invasion of Mahonia bealei in the Southeastern United States

Woodlots are forest islands embedded within an urban matrix, and often represent the only natural areas remaining in suburban areas. Woodlots represent critical conservation areas for native plants, and are important habitat for wildlife in urban areas. Invasion by non-indigenous (NIS) plants can alter ecological structure and function, and may be especially severe in remnant forests where NIS propagule pressure is high. Woody shrubs in the Family Berberidaceae have been well documented as invaders of the forest–urban matrix in North America. Mahonia bealei (Berberidaceae) is a clonal shrub native to China, and is a popular ornamental in the Southeastern United States. Mahoni bealei is listed as “present” on some local and state floras, but almost nothing is known regarding its invasion potential in the United States. We sampled 15 woodlots in Clemson, South Carolina, to assess the invasion of M. bealei and other woody non-indigenous species (NIS). M. bealei invaded 87% of the woodlots surveyed and species richness of NIS on these woodlots varied from 5 to 14. Stepwise-multiple regression indicated that less canopy cover and older M. bealei predicted greater abundance of M. bealei , and that not all subdivisions were equally invaded (P < 0.0001; r² = 0.88). The impact of M. bealei on native flora and fauna may be considerable, and it is likely to continue to spread in the Southeastern United States. M. bealei should be recognized as an aggressive invader in the Southeastern United States, with the potential for negative impacts on native flora and fauna.