Effect of quinclorac on auxin-induced growth, transmembrane proton gradient and ethylene biosynthesis in Echinochloa spp.

1998 ◽  
Vol 25 (7) ◽  
pp. 851 ◽  
Author(s):  
Nuria Lopez-Martinez ◽  
Richard H. Shimabukuro ◽  
Rafael De Prado
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Atpase Activity ◽  
Cell Elongation ◽  
Acc Synthase ◽  
Ethylene Biosynthesis ◽  
Elongation Growth ◽  
Ethylene Formation ◽  
Acc Content ◽  
Stimulation Of

The mechanism of action of quinclorac and its selectivity between rice and resistant (R), intermediately tolerant (I) and susceptible (S) Echinochloa spp. were investigated. The effect on the cell membrane potential (Em), stimulation of cell elongation growth, ACC production and ethylene formation were examined to verify the auxin characteristics of quinclorac and the possible mechanism of selectivity. Quinclorac did not induce cell elongation growth, neither did it cause hyperpolarization of Em due to the stimulation of H+ -ATPase activity. Quinclorac increased ethylene biosynthesis by increasing the ACC content in susceptible plants, possibly by affecting the autonomous auxin-regulated ACC synthase gene. Increased ethylene biosynthesis was correlated with the phytotoxicity of quinclorac. Ethylene biosynthesis due to quinclorac treatment in I and S biotypes increased 3 and 7 times, respectively, but quinclorac treatment had no effect on ethylene biosynthesis in R Echinochloa spp. and rice at the applied dosages. Quinclorac caused an increase of ACC concentration in the S biotype that was 2.5-fold more than the control. The addition of an ethylene biosynthesis inhibitor decreased the phytotoxicity of quinclorac. The mechanism of selectivity between susceptible and tolerant species/biotypes may be related to the formation of HCN as a coproduct during the stimulation of the ethylene biosynthesis caused by the herbicide only in susceptible grasses.

scholarly journals Inhibition of Ethylene Biosynthesis and Action in Cut Carnations (Dianthus caryophyllus L.) by Aminotriazole

1994 ◽  
Vol 119 (2) ◽  
pp. 282-287 ◽  
Author(s):  
Steven A. Altman ◽  
Theophanes Solomos
Keyword(s):  
Morphological Changes ◽  
Dianthus Caryophyllus ◽  
Acc Synthase ◽  
Ethylene Biosynthesis ◽  
Vase Life ◽  
Ethylene Evolution ◽  
Dependent Inhibition ◽  
Ethylene Action ◽  
Exogenous Ethylene ◽  
Acc Content

Treating `Elliott's White' cut carnations with 50 or 100 mm aminotriazole for 4 days inhibits the respiratory climacteric and significantly extends vase life. Aminotriazole induced time- and concentration-dependent inhibition of ethylene evolution and onset of the ethylene climacteric by inhibiting ACC synthase activity. Flowers treated with 50 or 100 mm aminotriazole for 2 days exhibited concentration-dependent increases in ethylene evolution, respiratory activity, ACC synthase activity, and petal ACC content in response to the application of exogenous ethylene at 10 μl·liter-1. Senescence-associated morphological changes, increased ACC synthase activity, ACC content, and ethylene evolution were completely inhibited in flowers treated for 4 days with 100 mm aminotriazole. Although treatment with 50 mm aminotriazole for 4 days did not completely inhibit components of the ethylene biosynthetic pathway, no morphological or respiratory responses to the application of exogenous ethylene at 10 μl·liter-1 were observed, a result indicating that prolonged aminotriazole treatment inhibited ethylene action. Chemical names used: 3-1H-amino-1,2,4-triazole-1-yl (aminotriazole), 1-aminocyclopropane-1-carboxylic acid (ACC).

scholarly journals Ethylene Biosynthesis during Peach Fruit Development

1991 ◽  
Vol 116 (2) ◽  
pp. 274-279 ◽  
Author(s):  
P. Tonutti ◽  
P. Casson ◽  
A. Ramina
Keyword(s):  
Carboxylic Acid ◽  
Growth And Development ◽  
Prunus Persica ◽  
Acc Synthase ◽  
Ethylene Biosynthesis ◽  
Full Bloom ◽  
Ethylene Evolution ◽  
Peach Fruit ◽  
Stages Of Growth ◽  
Acc Content

Ethylene evolution and ACC levels were determined throughout the growth and development of peach fruit (Prunus persica L. Batsch cv. Redhaven). In the four stages of growth (I, II, III, IV), as indicated by weekly monitoring of fresh (FW) and dry (DW) weight accumulation, ethylene biosynthesis in whole fruit decreased during FWI and remained almost undetectable during FWII and FWIII. In pericarp disks, ethylene evolution followed the same trend, although a peak at 78 days after full bloom and a slight increase before the onset of the climacteric were observed. The high rates of ethylene evolution were associated with a concurrent increase in ACC content. Enhancement of ACC synthase and ethylene-forming enzyme (EFE) activities was responsible for the peak of ethylene evolution detected before the beginning of FWIII and DWIII. At the climacteric, which occurred at the FWIII-FWIV transition, sequential events were observed in different fruit tissues. An increase of ethylene production in the mesocarp preceded the onset of the climacteric rise in whole fruit. The high amount of ethylene detected during the climacteric appeared to be related to increased EFE activity in the epicarp. Chemical name used: 1-aminocyclopropane-1-carboxylic acid (ACC).

Antagonism by Clopyralid of Picloram-Induced Ethylene Biosynthesis in Rapeseed Plants

1991 ◽  
Vol 46 (11-12) ◽  
pp. 957-962
Author(s):  
J. Christopher Hall ◽  
Mira Soni
Keyword(s):  
Carboxylic Acid ◽  
De Novo ◽  
Subsequent Development ◽  
Acc Synthase ◽  
Ethylene Biosynthesis ◽  
De Novo Synthesis ◽  
Ethylene Evolution ◽  
Significant Difference ◽  
Acc Conversion ◽  
Stimulation Of

The effect of clopyralid pretreatment (500 g/ha) on picloram-induced ethylene, ACC (1-aminocyclopropane-l-carboxylic acid), and MACC [l-(malonylamino)-cyclopropane-1-carboxylic acid] was measured in rapeseed plants that were treated with 50 or 100 g/ha of picloram. In contrast to plants that did not receive a clopyralid pretreatment, ethylene biosynthesis was significantly reduced in plants pretreated with clopyralid prior to picloram. Picloram- induced levels of ACC also were significantly reduced in plants receiving pretreatment with clopyralid. In contrast, there was no difference between the levels of MACC in plants that were and were not pretreated with clopyralid. Therefore, the mechanism by which clopyralid pretreatment interferes with picloram-induced synthesis of both ACC and ethylene may be manifested through the blocking of de novo synthesis of ACC synthase normally stimulated by picloram. The lack of significant difference in MACC levels between plants that were and were not pretreated with clopyralid precludes the stimulation of enhanced ACC conversion to MACC as an exclusive mechanism of clopyralid’s antidoting activity. It is likely that the rate of picloram-induced ACC synthesis by plants receiving pretreatment is within their capacity to convert ACC to MACC, thereby limiting the substrate available for conversion to ethylene. In contrast, it appears that the extent of ACC synthesis by plants receiving no pretreatment supersedes their capacity for conversion to MACC. thereby resulting in greatly enhanced rates of ethylene evolution and subsequent development of injury symptoms.

Antagonism by Clopyralid of Picloram-Induced Ethylene Biosynthesis in Rapeseed Plants

1991 ◽  
Vol 46 (9-10) ◽  
pp. 957-962 ◽  
Author(s):  
J. Christopher Hall ◽  
Mira Soni
Keyword(s):  
Carboxylic Acid ◽  
De Novo ◽  
Subsequent Development ◽  
Acc Synthase ◽  
Ethylene Biosynthesis ◽  
De Novo Synthesis ◽  
Ethylene Evolution ◽  
Significant Difference ◽  
Acc Conversion ◽  
Stimulation Of

Abstract The effect of clopyralid pretreatment (500 g/ha) on picloram-induced ethylene, ACC (1-aminocyclopropane-1-carboxylic acid), and MACC [1-(malonylamino)-cyclopropane-1-carboxylic acid] was measured in rapeseed plants that were treated with 50 or 100 g/ha of picloram. In contrast to plants that did not receive a clopyralid pretreatment, ethylene biosynthesis was significantly reduced in plants pretreated with clopyralid prior to picloram. Piclo­ram-induced levels of ACC also were significantly reduced in plants receiving pretreatment with clopyralid. In contrast, there was no difference between the levels of MACC in plants that were and were not pretreated with clopyralid. Therefore, the mechanism by which clopyralid pretreatment interferes with picloram-induced synthesis of both ACC and ethylene may be manifested through the blocking of de novo synthesis of ACC synthase normally stimulated by picloram. The lack of significant difference in MACC levels between plants that were and were not pretreated with clopyralid precludes the stimulation of enhanced ACC conversion to MACC as an exclusive mechanism of clopyralid’s antidoting activity. It is likely that the rate of picloram-induced ACC synthesis by plants receiving pretreatment is within their capacity to convert ACC to MACC, thereby limiting the substrate available for conversion to ethylene. In contrast, it appears that the extent of ACC synthesis by plants receiving no pretreatment su­persedes their capacity for conversion to MACC, thereby resulting in greatly enhanced rates of ethylene evolution and subsequent development of injury symptoms.

scholarly journals Chloride-ion stimulation of the tonoplast H+-translocating ATPase from Hevea brasiliensis (rubber tree) latex. A dual mechanism

1985 ◽  
Vol 226 (1) ◽  
pp. 85-94 ◽  
Author(s):  
B P Marin ◽  
X Gidrol
Keyword(s):  
Membrane Potential ◽  
Atpase Activity ◽  
Hevea Brasiliensis ◽  
Rubber Tree ◽  
Electrical Potential ◽  
Chloride Ion ◽  
The Other ◽  
Potential Difference ◽  
Dual Mechanism ◽  
Stimulation Of

The effect of Cl- and other anions on the tonoplast H+-translocating ATPase (H+-ATPase) from Hevea brasiliensis (rubber tree) latex was investigated. Cl- and other anions stimulated the ATPase activity of tightly sealed vesicles prepared from Hevea tonoplast, with the following decreasing order of effectiveness: Cl- greater than Br- greater than SO4(2-) greater than NO3-. As indicated by the changes of the protonmotive potential difference, anion stimulation of tonoplast H+-ATPase was caused in part by the ability of these anions to dissipate the electrical potential. This interpretation assumes not a channelling of these anions against a membrane potential, negative-inside, but a modification of the permeability of these ions through the tonoplast membrane. In addition, Cl- and the other anions stimulated the ATPase activity solubilized from the tonoplast membrane. Consequently, the tonoplast H+-pumping ATPase can be considered as an anion-stimulated enzyme. These results are discussed in relation to various models described in the literature for the microsomal H+-ATPase systems claimed as tonoplast entities.

In Silico Study of Ethylene Biosynthesis: Seeking New Effectors of ACC Synthase and ACC Oxidase

2016 ◽  
Vol 11 (3) ◽  
pp. 346-356
Author(s):  
Nada Ayadi ◽  
Sarra Aloui ◽  
Rabeb Shaiek ◽  
Oussama Rokbani ◽  
Faten Raboud ◽  
...  
Keyword(s):  
In Silico ◽  
Acc Oxidase ◽  
Acc Synthase ◽  
Ethylene Biosynthesis ◽  
In Silico Study

Use of Isolated Tight Epithelia to Study the Site and Mode of Drug Action on Cell Membrane Transport: Effect of the Antipsychotic Agent Trifluoperazine

1990 ◽  
Vol 17 (3) ◽  
pp. 224-227
Author(s):  
Henning F. Bjerregaard
Keyword(s):  
Cell Membrane ◽  
Toxic Effect ◽  
Membrane Transport ◽  
Antipsychotic Agent ◽  
Na Transport ◽  
Tight Epithelia ◽  
Acute Toxic Effect ◽  
Cell Membrane Transport ◽  
Dose Dependent ◽  
Stimulation Of

The aim of the present study was to investigate the site and mode of trifluoperazine (TFP) action on cell membrane transport by the use of isolated frog skin. This cellular system gives access to the apical (outer) and basolateral (inner) membranes of the polarised epithelial cells. Both apical and basolateral TFP addition induced a dose-dependent stimulation of Na transport, and depolarised the cellular potential. The data indicate that TFP acts by increasing the Na permeability of the apical membrane. However, the mechanisms localised in the apical and basolateral membranes are quite different. Basolateral TFP addition increased Na transport due to a stimulation of PGE2 synthesis, whereas apical TFP addition abolished Na inhibition of the apical Na channels, and thereby enhanced the Na transport. An acute toxic effect on the electrophysiological parameters was noted after addition of high apical TFP concentrations (50–100μM). This toxic effect was dependent on the presence of Na in the apical solution.

scholarly journals Cytoplasmic [Ca2+] and intracellular pH in lymphocytes. Role of membrane potential and volume-activated Na+/H+ exchange.

1987 ◽  
Vol 89 (2) ◽  
pp. 185-213 ◽  
Author(s):  
S Grinstein ◽  
S Cohen
Keyword(s):  
Protein Kinase C ◽  
Membrane Potential ◽  
Protein Kinase ◽  
Intracellular Ph ◽  
Enzyme Treatment ◽  
Membrane Hyperpolarization ◽  
Kinase C ◽  
Free Media ◽  
Stimulation Of

The effect of elevating cytoplasmic Ca2+ [( Ca2+]i) on the intracellular pH (pHi) of thymic lymphocytes was investigated. In Na+-containing media, treatment of the cells with ionomycin, a divalent cation ionophore, induced a moderate cytoplasmic alkalinization. In the presence of amiloride or in Na+-free media, an acidification was observed. This acidification is at least partly due to H+ (equivalent) uptake in response to membrane hyperpolarization since: it was enhanced by pretreatment with conductive protonophores, it could be mimicked by valinomycin, and it was decreased by depolarization with K+ or gramicidin. In addition, activation of metabolic H+ production also contributes to the acidification. The alkalinization is due to Na+/H+ exchange inasmuch as it is Na+ dependent, amiloride sensitive, and accompanied by H+ efflux and net Na+ gain. A shift in the pHi dependence underlies the activation of the antiport. The effect of [Ca2+]i on Na+/H+ exchange was not associated with redistribution of protein kinase C and was also observed in cells previously depleted of this enzyme. Treatment with ionomycin induced significant cell shrinking. Prevention of shrinking largely eliminated the activation of the antiport. Moreover, a comparable shrinking produced by hypertonic media also activated the antiport. It is concluded that stimulation of Na+/H+ exchange by elevation of [Ca2+]i is due, at least in part, to cell shrinking and does not require stimulation of protein kinase C.

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