Stimulation of ethylene or ethane production by malformin

Malformin stimulated ethylene production of Phaseolus vulgarisL. seedlings and explants. However, when malformin was vacuum-infiltratedinto apical bud sections, the production of ethylene was inhibited,ethane production was stimulated and the sections became softand pliable; in pure oxygen, ethylene production was- stimulatedand the sections remained firm. Prolonged stimulation of ethaneproduction by malformin-treated sections required oxygen. Indoleaceticacid (IAA) had no effect on the stimulation of ethane productionby malformin-infiltrated tissues; malformin and IAA stimulatedethylene production synergistically at the same time that malformininducedethane production had increased markedly. ¹This work was supported by grant GB-7158 from the NationalScience Foundation. ²Journal Paper No. 3560 of the Purdue Agricultural ExperimentStation. (Received July 23, 1969; )     

Potentiation and inhibition of the effects of 2-chloroethylphosphonic Acid by malformin

Malformin completely inhibited Ethrel-induced swelling and fresh weight increase on the basal stem portion of Phaseolus vulgaris L. cuttings, but markedly potentiated Ethrel- or ethylene-induced abscission. With regard to abscission, malformin reacted synergistically with ethylene and dark aging, and in a manner which appeared to differ from that of ethylene and dark aging. The numerous effects of malformin on plant growth and development cannot be explained in simple terms of enhanced ethylene production.     

Phytochrome involvement in stimulation and alleviation of inhibition of plant growth by malformin

Stimulation of stem elongation on green cuttings of Phaseolus aureus by malformin occurred only in red light and was specifically reversible by subsequent treatment with far red radiation. Inhibition of stem elongation of etiolated cuttings by malformin in the dark was alleviated by red light and was repeatedly reversible with far red irradiation. A direct or indirect effect of malformin on phytochrome action was suggested.     

Stimulation of mitoplast respiration by mitochondrial porin

Mitochondrial porin (2 ng/ml) being added to the rat liver mitoplasts considerably stimulates the respiration in the third and uncoupled states. As the same effect was observed previously with the addition of outer membrane fraction to the mitoplast suspension, it is concluded that mitochondrial porin participates in regulation of the mitochondria respiration and, probably, is the natural activator of the ADP/ATP carrier function.     

Mediation of a plant response to malformin by ethylene

Malformin and ethylene stimulate abscission of the primary leaves of Phaseolus aureus Roxb. in the dark, and abscission stimulation by both compounds is inhibited by indeleacetic acid and CO₂. Ethylene production by malformin-treated buds is stimulated within 4 hours. and up to 8 days, after treatment. Malformin-induced growth disturbances in P. vulgaris L. and abscission in P. aureus are considered mediated by ethylene. Although root curvatures of Zea mays L. are induced by both malformin and ethylene, and malformin is inhibited by CO₂, ethylene production is not stimulated by malformin. A role of ethylene in root curvatures induced by malformin is neither proposed nor disproved.     

Ethylene and ethane production in response to salinity stress

Abstract Ethylene and ethane production in mung bean hypocotyl sections were evaluated as possible indicators of stress due to contact with four salts that are common in natural sites. Ethylene production decreased with increasing concentrations of applied NaCl and KCl. When CaCl₂ was applied, the ethylene evolution was greater. However, when MgCl₂ was applied, ethylene evolution remained high then decreased and at higher salt concentrations again showed an increase. NaCl (up to 0.1 kmol m^?1) and KCl (up to 0.5 kmol m^?3) caused a concentration-dependent increase in ethane production. The ethane production with CaCl₂ was the lowest among the salts tested and only a minute increase was noticed with the increase of concentration from 0.01 to 1 kmol m^?3. Ethane production showed a distinct maximum at 0.2 kmol m^?3 MgCl₂. The introduction of 0.01 kmol m^?3 CaCl₂, as well as anaerobic conditions obtained by purging vials with N₂, eliminated that high ethane production. Respiratory activity of the mung bean hypocotyl sections in MgCl₂ concentrations from 0 to 0.5 kmol m^?3 was correlated with ethane but not with ethylene production. The ethane/ethylene ratio showed three patterns for the four salts tested.     

Stimulation and inhibition of myoblast differentiation by hormones

The growth and differentiation of L6 myoblasts are subject to control by two proteins secreted by cells of the Buffalo rat liver line. The first of these, rat insulinlike growth factor-II (formerly designated multiplication stimulating activity) is a potent stimulator of myoblast proliferation and differentiation, as well as associated processes such as amino acid uptake and incorporation into protein, RNA synthesis, and thymidine incorporation into DNA. In addition, this hormone causes a significant decrease in the rate of protein degradation. All of these actions seem to be attributable to a single molecular species, although their time courses and sensitivity to the hormone differ substantially. The second protein, the differentiation inhibitor (DI), is a nonmitogenic inhibitor of all tested aspects of myoblast differentiation, including fusion and the elevation of creatine kinase. Indirect immunofluorescence experiments demonstrated that DI also blocks accumulation of myosin heavy chain and myomesin. Upon removal of DI after 72 h incubation, all of these effects were reversed and normal myotubes containing the usual complement of muscle-specific proteins were formed. Thus, this system makes it possible to achieve specific stimulation or inhibition of muscle cell differentiation by addition of purified proteins to cloned cells in serum-free medium.     

Stimulation and inhibition of myoblast differentiation by hormones

Summary The growth and differentiation of L6 myoblasts are subject to control by two proteins secreted by cells of the Buffalo rat liver line. The first of these, rat insulinlike growth factor-II (formerly designated multiplication stimulating activity) is a potent stimulator of myoblast proliferation and differentiation, as well as associated processes such as amino acid uptake and incroporation into protein, RNA synthesis, and thymidine incorporation into DNA. In addition, this hormone causes a significant decrease in the rate of protein degradation. All of these actions seem to be attributable to a single molecular species, although their time courses and sensitivity to the hormone differ substantially. The second protein, the differentiation inhibitor (DI), is a nonmitogenic inhibitor of all tested aspects of myoblast differentiation, including fusion and the elevation of creatine kinase. Indirect immunofluorescence experiments demonstrated that DI also blocks accumulation of myosin heavy chain and myomesin. Upon removal of DI after 72 h incubation, all of these effects were reversed and normal myotubes containing the usual complement of muscle-specific proteins were formed. Thus, this system makes it possible to achieve specific stimulation or inhibition of muscle cell differentiation by addition of purified proteins to cloned cells in serum-free medium. This work was supported by a Muscular Dystrophy Association Postdoctoral Fellowship (M. J. E.-H.), U.S. Public Health Service Grant HL-11551 and AG-00629 (J. R. F.) and AM-28433 (B. M. V.), and a grant from the Muscular Dystrophy Association (J. R. F.).     

Stimulation by hexose esters of lactate production by rat erythrocytes,insensitivity to 3-O-methyl-D-glucose and inhibition by 2-deoxy-D-glucose and its tetraacetic ester

Selected esters of D-glucose were recently proposed as tools to provide the sugar to cells, whilst bypassing the carrier system for hexose transport across the plasma membrane. In the present study, -D-glucose pentaacetate, -D-glucose pentaacetate, -D-mannose pentaacetate and, to a lesser extent, 6-O-acetyl-D-glucose, all tested at a 1.7 mM concentration, were found to increase lactate production above basal value in rat erythrocytes. Over 90 min incubation, the increment in lactate production ranged from about 1.2 (-D-glucose pentaacetate) to 0.6 (6-O-acetyl-D-glucose) mol/l of erythrocytes. Little or no change in lactate production was observed in cells exposed to -L-glucose pentaacetate, -D-glucose pentaethylsuccinate, -D-galactose pentaacetate or -D-galactose pentaacetate. The metabolic response to -D-glucose pentaacetate was resistant to 3-O-methyl-D-glucose (10-80 mM) which suppressed, however, that evoked by D-glucose. D-mannoheptulose (10 mM) virtually failed to affect the response to D-glucose and its pentaacetate ester. On the contrary, 2-deoxy-D-glucose (10.6 mM) inhibited to the same relative extent (55% decrease) lactate production in erythrocytes exposed to either unesterified D-glucose or -D-glucose pentaacetate. The tetraacetic ester of 2-deoxy-D-glucose was more efficient than unesterified 2-deoxy-D-glucose in inhibiting lactate production from -D-glucose pentaacetate. It is proposed that selected esters of saccharides represent useful tools to bypass defects in hexose transport, and to increase their nutritional or therapeutic efficiency.     

Phytochrome involvement in the induction of resistance to dark abscission by malformin

The active portion of the visible spectrum which is required for malformin to produce leaves which are resistant to dark abscission from cuttings of Phaseolus aureus is red light. Abscission resistance was partially to almost completely lost by far irradiation prior to dark incubation. Although Ethrel, an ethylene releasing compound, stimulated dark abscission of resistant and control leaves, resistance was not lost because control leaves always abscised at a greater rate. The participation of phytochrome in the induction of abscission resistance by malformin is indicated.Abbreviations Pfr far-red absorbing form of the phytochrome system - R red radiation - FR far-red radiation - D dark     

Stimulation of tumor-cell respiration by inhibitors of pyruvate kinase.

In a model system consisting of highly coupled rat liver mitochondria respiring in the presence of substrate, pyruvate kinase, phosphoenolpyruvate, ATP, hexokinase and glucose, the increase in the mitochondrial concentration results in a progressive decrease in the activity of pyruvate kinase. These results are in accord with a role of pyruvate kinase as a determinant of glycolytic activity by competing with mitochondrial oxidative phosphorylation for the available ADP. The addition of adequate amounts of the amino acids, cysteine, alanine and phenylalanine, known as inhibitors of pyruvate kinase, to living Ehrlich ascites tumor cell suspensions results in a stimulation of the respiratory rate and in a decrease of the glycolytic rate of the cells. Concomitant with these changes, there is an accumulation of intracellular phosphoenolpyruvate and ADP, and a decrease in pyruvate and ATP. These results provide additional evidence for paying attention to pyruvate kinase as another key enzyme whose properties and activities may be major determinants for the control of glycolysis and the Crabtree and Pasteur effects of tumor cells.     

Stimulation of cell growth and inhibition of prostacyclin production by heparin in human umbilical vein endothelial cells

We characterized human umbilical vein (HUV) endothelial cells as to cell growth and prostacyclin production to get a better understanding of the properties of endothelial cells. Endothelial cell growth supplement (ECGS) and basic fibroblast growth factor (FGF) stimulated HUV endothelial cell growth. Heparin further enhanced the cell growth stimulated by ECGS, but not the cell growth stimulated by FGF or in the absence of these growth factors. In the presence of ECGS, the prostacyclin-producing capacity of the cells was inhibited by heparin. However, in the presence of FGF of in the absence of growth factors, heparin did not inhibit prostacyclin production. Therefore, it is likely that there is a specific correlation between heparin and growth factors for endothelial cells in the blood vessel to maintain nonthrombogenicity properly. Heparin-treated cultures may not be suitable for some examinations of prostacyclin production by vascular endothelial cells.