Stimulation of Growth and Nucleic Acid Biosynthesis at Low Concentration of Abscisic Acid in Tissue Culture of Spinacia oleracea

The effect of abscisic acid on growth, ultrastructure and nucleic acid biosynthesis was studied in tissue culture of spinach (Spinacia oleracea L.). Low concentration (0.01 mg l^?1) of abscisic acid increased fresh and dry weight of calluses, whereas 1.0 mg l^?1 was inhibitory. The stimulating effect was observed only in the presence of a relatively high concentration of kinetin (1 mg l^?1). The inhibitory effect was partly overcome by the same kinetin concentration. The low concentration of abscisic acid probably accelerated the induction of callus growth after subculture and stimulated cell division in the exponential phase of growth. Electron microscopy showed the presence of numerous polysomes and rough endoplasmic reticulum in callus cells grown at the stimulating abscisic acid concentration. Control cells and cells at the inhibitory concentration had slightly hyaline cytoplasm and were more vacuolated. Incubation of callus tissue with ³²P in the presence of stimulating concentration of abscisic acid showed a significant increase in the rate of biosynthesis of all nucleic acid classes after 8 h, whereas inhibitory concentration produced a decrease in ³²P incorporation. However, when the tissue was grown in the presence of abscisic acid for 20 days, both concentrations decreased the rate of nucleic acid biosynthesis, as compared to the controls.     

Intracellular calcium buffering capacity in isolated squid axons

Changes in ionized calcium were studied in axons isolated from living squid by measuring absorbance of the Ca binding dye Arsenazo III using multiwavelength differential absorption spectroscopy. Absorption changes measured in situ were calibrated in vitro with media of ionic composition similar to axoplasm containing CaEGTA buffers. Calcium loads of 50-2,500 μmol/kg axoplasm were induced by microinjection, by stimulation in 112 mM Ca seawater, or by soaking in choline saline with 1-10 mM Ca. Over this range of calcium loading of intact axoplasm, the ionized calcium in the axoplasm rose about 0.6 nM/μM load. Similar loading in axons preteated with carbonyl cyanide 4- trifluoromethoxyphenylhydrazone (FCCP) to inhibit the mitochondrial proton gradient increased ionized calcium by 5-7 percent of the imposed load, i.e. 93-95 percent of the calcium load was buffered by a process insensitive to FCCP. This FCCP- insensitive buffer system was not saturated by the largest calcium loads imposed, indicating a capacity of at least several millimolar. Treatment of previously loaded axons with FCCP or apyrase plus cyanide produced rises in ionized calcium which could be correlated with the extent of the load. Analysis of results indicated that, whereas only 6 percent of the endogenous calcium in fresh axons is stored in the FCCP-sensitive (presumably mitochondrial) buffer system, about 30 percent of an imposed exogenous load in the range of 50-2,500 μM is taken up by this system.     

Ueber die Scleranthen des Aetna und der Nebroden

Ohne Zusammenfassung     

Evidence for an early G1 ionic event necessary for cell cycle progression and survival in the MCF-7 human breast carcinoma cell line

The mechanism of the G0/G1 arrest and inhibition of proliferation by quinidine, a potassium channel blocker, was investigated in a tissue culture cell line, MCF-7, derived from a human breast carcinoma. The earliest measurable effect of quinidine on the cell cycle was a decrease in the fraction of cells in S phase at 12 hr, followed by the accumulation of cells in G1/G0 phases at 30 hr. Arrest and release of the cell cycle established quinidine as a cell synchronization agent, with a site of arrest in early G1 preceding the lovastatin G1 arrest site by 5–6 hr. There was a close correspondence among the concentration-dependent arrest by quinidine in G1, depolarization of the membrane potential, and the inhibition of ATP-sensitive potassium currents, supporting a model in which hyperpolarization of the membrane potential and progression through G1 are functionally linked. Furthermore, the G1 arrest by quinidine was overcome by valinomycin, a potassium ionophore that hyperpolarized the membrane potential in the presence of quinidine. With sustained exposure of MCF-7 cells to quinidine, expression of the Ki67 antigen, a marker for cells in cycle, decreased, and apoptotic and necrotic cell death ensued. We conclude that MCF-7 cells that fail to progress through the quinidine-arrest site in G1 die. J. Cell. Physiol. 176:456-464, 1998. © 1998 Wiley-Liss, Inc.     

Flora des Etna

Ohne Zusammenfassung     

Ausflug auf den grossen Bösenstein (7731 F.) (17. August 1868.)

Ohne Zusammenfassung