Chromosome length values in digenomic buttercups [Ranunculaceae] and the relation to DNA content

Root-tip chromosome complement length ratios were determined in F1 hybrids combinining two haploid (n = 8) genomes each from different species, to form a series AB, AC, AD, ... AI. The observed values, for the length ratios B/A, C/A, etc., ranged from 0.53 to 1.0. It is noted that the values form a quasilinear distribution, with a slope of 1.0, when plotted against the known 4C DNA values of the species having a range from appr. 1.1 to 2.2 × 10^?11 g. Also observed, but not numerically evaluated was some apparently related variation in chromosome “width”. DNA-related variation in root-tip chromosome size in these buttercups may be three-dimensional; however, the magnitude of the observed length differentials and the 1∶1 correlation with DNA content suggest that it occupies predominantly the first dimension.     

Extracellular ATP and adenosine modulate tumor necrosis factor-induced lysis of L929 cells in the presence of actinomycin D

Extracellular ATP in concentrations of 0.5 to 2.5 mM modulates TNF-induced cytolysis of L929 cells in the presence of actinomycin D. When present throughout the entire assay period, it inhibits the TNF-induced cytolysis. ADP was less active whereas AMP and GTP were nonreactive. However, inhibition was also achieved by adenosine that was nearly as active as ATP. Yet, the inhibitory effect of ATP was not due to hydrolysis by ectoenzymes to form adenosine. Thus, the nonhydrolyzable ATP analogue adenyl(beta-gamma-methylendiphosphate) was equally effective in inhibiting TNF-induced cytolysis. Moreover, no conversion of ATP into adenosine was observed during the entire assay period. However, inhibition no longer occurred when the TNF and ATP containing medium was removed after 5 h and replaced by a fresh medium containing TNF and no ATP. We now observed substantial enhancement of the TNF-induced cytolysis by ATP. Finally, treatment with N6-(R-phenylisopropyl)adenosine or with aminophylline, which are thought to downregulate adenosine receptors and to prevent binding of ligands to adenosine receptors, respectively, abolishes adenosine and ATP-mediated inhibition. Again, substantial enhancement of the TNF-induced cytolysis was observed by ATP and only a minor effect by adenosine. The results together suggest that ATP interacts with purinoceptors on the plasma membrane and is capable to enhance and inhibit TNF-induced cytolysis under appropriate conditions. The outcome of the ATP-induced modulation may be influenced by adenosine receptors.