Minor xanthones of Hypericum mysorense

2-Hydroxyxanthone, 1,7-dihydroxyxanthone, 1-hydroxy-7-methoxyxanthone, 6,7-dimethoxy-1-hydroxyxanthone and a new natural product, 2-hydroxy-3-methoxyxanthone, have been isolated and characterized from the phenolic fraction of the chloroform extract of the timber of Hypericum mysorense. The presence of simple xanthones in this genus supports the classification of Hypericum in the subfamily Hypericoideae in Guttiferae.     

The bps signal: Embryonic arrest from an auxin-independent mechanism in bypass triple mutants

Long-distance signaling is essential for coordination of plant development and environmental responses. We originally isolated a tiny mutant named bypass1 (bps1), which has defects in shoot and root development. The bps1 roots overproduce a mobile signal (bps signal) that arrests both root and shoot development. Our recent study demonstrated that all three BPS gene family members prevent ectopic synthesis of the same bps signal.bps multiple mutants show progressively more severe developmental defects. An embryogenesis analysis revealed abnormal cell divisions in all meristem lineages of bps triple mutants. These defects appear to be auxin independent, and arise prior to changes in PLT1 and PLT2 expression.     

Spectroscopic and potentiometric evidence for the stabilization of a bent structure of octapeptides by Cu(II) ions

Syntheses and the results of a potentiometric and spectrophotometric study at 25°C and an ionic strength of 0.10 mol dm^?3 (KNO₃) of the H ⁺ and Cu²⁺ complexes of two pairs of tetra- and octapeptides are reported. The peptides, Gly-Gly-Pro-Gly and (Gly-Gly-Pro-Gly)₂, and Gly-Gly-Pro-Lys and (Gly-Gly-Pro-Lys)₂, are models for the biologically active octapeptide with antitumor activity, dog tuftsinyltuftsin. The results clearly demonstrate participation of the ?-NH₂ group of -Lys- in metal ion coordination from below pH 6 and, with the octapeptides at high pH, suggest the presence of a bent conformation with a large chelate ring spanning the two ends of the peptide chain.     

Interacting Genes Control Glycerol-3-Phosphate Dehydrogenase Expression in Developing Cerebellum of the Mouse

The cerebellum of BALB/cJ mice has approximately 2.5 times as much glycerol-3-phosphate dehydrogenase (GPDH) as that of C57BL/6J mice. This difference in enzyme levels, which positively correlates with similar differences in the levels of hybridizable GPDH mRNA, is controlled by at least two unlinked regulatory loci and the structural gene, Gdc-1, located on chromosome 15. These regulatory loci, which act predominantly during the second and third weeks of postnatal cerebellar development and differentiation, have been separated from each other in the CXB recombinant inbred strains of mice. One regulatory locus, Gdcr-1, although unlinked to the structural gene, has an allele in BALB/c mice that preferentially enhances expression of the BALB/c structural allele at Gdc-1. The other locus, Gdcr-2, which may or may not be single, enhances GPDH expression at Gdc-1 irrespective of the allele present, as is commonly observed for loci acting from a distance. Measurements of GPDH mRNA in the recombinant inbred mice suggest that these regulatory genes act by modulating mRNA levels. Accordingly, the regulation of GPDH expression in the cerebellum of mice depends on a complex interaction of unlinked regulatory elements with regulatory elements near the structural gene. Furthermore, since the Gdc-1 locus is expressed in virtually every tissue of the mouse except blood and since the observed genetic variation is restricted to the cerebellum, it is likely that other tissues will have their own distinctive genetic mechanisms for modulating Gdc-1 expression.     

Activation of NADPH-dependent superoxide production in a cell-free system by sodium dodecyl sulfate

Sodium dodecyl sulfate (SDS) elicits the production of superoxide (O2-) by a cell-free system represented by sonically disrupted guinea pig peritoneal macrophages. O2- generation requires NADPH and a heat-sensitive cellular component, is proportional to the amount of macrophage protein, and exhibits a pH optimum of 6.5-7. The kinetic parameters of the SDS-stimulated enzyme are: Km (+/- S.E.) = 0.0367 +/- 0.003 mM NADPH and Vmax (+/- S.E.) = 73.46 +/- 9.09 nmol O2-/mg of protein/min. O2- production is dependent on the cooperation between a particulate subcellular component sedimentable at 48,000 X g and a cytosolic factor present in the 48,000 X g supernatant. The activity of both components is destroyed by heating at 80 degrees C. Pretreatment of intact macrophages with phorbol myristate acetate results in the partial removal of the requirement for cytosolic factor; SDS is now capable of activating the isolated 48,000 X g pellet. Among a large number of anionic, cationic, and nonionic detergents tested, only the anionic detergents SDS and sodium dodecyl sulfonate are capable of eliciting O2- production in the cell-free system, SDS being the more potent stimulant. It is proposed that the structural requirements that make these compounds capable of activating the O2- forming NADPH oxidase in a cell-free system are the presence of an anionic polar head and a long hydrophobic alkyl tail. We suggest that sodium salts of long chain unsaturated fatty acids that were found by us to be capable of stimulating O2- production in a cell-free system (Bromberg, Y., and Pick, E. (1984) Cell. Immunol. 88, 213-221) owe their activity to the fact that they function as anionic detergents.     

Effect of adherence,cell morphology,and lipopolysaccharide on potassium conductance and passive membrane properties of murine macrophage J774.1 cells

Summary The effects of adherence, cell morphology, and lipopolysaccharide on electrical membrane properties and on the expression of the inwardly rectifying K conductance in J774.1 cells were investigated. Whole-cell inwardly rectifying K currents (K _i), membrane capacitance (C _m), and membrane potential (V _m) were measured using the patch-clamp technique. SpecificK _i conductance (G _K i, whole-cell Ki conductance corrected for leak and normalized to membrane capacitance) was measured as a function of time after adherence, and was found to increase almost twofold one day after plating. Membrane potential (V _m) also increased from –42±4 mV (n=32) to –58±2 mV (n=47) over the same time period.G _K i andV _m were correlated with each other;G _L (leak conductance normalized to membrane capacitance) andV _m were not. The magnitudes ofG _K i andV _m 15 min to 2 hr after adherence were unaffected by the presence of 100 m cycloheximide, but the increase inG _K iandV _m that normally occurred between 2 and 8 hr after adherence was abolished by cycloheximide treatment. Membrane properties were analyzed as a function of cell morphology, by dividing cells into three categories ranging from small round cells to large, extremely spread cells. The capacitance of spread cells increased more than twofold within one day after adherence, which indicates that spread cells inserted new membrane. Spread cells had more negative resting membrane potentials than round cells, butG _K i andG _L were not significantly different. Lipopolysaccharide-(LPS; 1 or 10 g/ml) treated cells showed increasedC _m compared to control cells plated for comparable times. In contrast to the effect of adherence, LPS-treated cells exhibited a significantly lowerG _K i than control cells, indicating that the additional membrane did not have as high a density of functionalG _K i channels. We conclude that both adherence and LPS treatment increase the total surface membrane area of J774 cells and change the density of Ki channels. In addition, this study demonstrates that membrane area and density of Ki channels can vary independently of one another.     

Apomorphine Does Not Alter Amphetamine-Induced Dopamine Release Measured in Striatal Dialysates

Amphetamine facilitates the release of dopamine from nerve terminals, but the mechanisms underlying this effect have not been fully delineated. The present experiments were designed to test the extent to which amphetamine-induced dopamine release is dependent on impulse flow and autoreceptor function in dopaminergic neurons. Rats were pretreated with a low dose of apomorphine (0.05 mg/kg) to inhibit dopamine neuronal activity, and the striatal dopaminergic response to amphetamine (0.5 mg/kg) was assessed by in vivo dialysis in freely moving animals. Consistent with previous results, apomorphine alone substantially decreased, whereas amphetamine increased, striatal dialysate dopamine concentrations. However, whereas apomorphine pretreatment decreased the locomotor response to amphetamine, the amphetamine-induced increase in dialysate dopamine was unaffected. These results indicate that amphetamine-facilitated dopamine release is independent of neuronal firing and autoreceptor regulation, consistent with the putative accelerative exchange-diffusion mechanism of amphetamine-induced dopamine release. Other possible mechanisms underlying the inhibitory effects of apomorphine on amphetamine locomotor activation are discussed.