scholarly journals Studies on 3-Indoleacetic Acid Metabolism. IV. Conjugation with Aspartic Acid and Ammonia as Processes in the Metabolism of Carboxylic Acids.

1957 ◽  
Vol 32 (6) ◽  
pp. 566-572 ◽  
Author(s):  
W. A. Andreae ◽  
Norman E. Good
Keyword(s):  
Aspartic Acid ◽  
Carboxylic Acids ◽  
Indoleacetic Acid ◽  
Acid Metabolism

Amino Acid Metabolism in Plants. V. Changes in Basic Indole Compounds and the Development of Tryptophan Decarboxylase Activity in Barley (Hordeum vulgare) during Germination and Seedling Growth

1974 ◽  
Vol 52 (8) ◽  
pp. 698-705 ◽  
Author(s):  
Elnora A. Schneider ◽  
F. Wightman
Keyword(s):  
Amino Acid ◽  
Shoot Growth ◽  
Indoleacetic Acid ◽  
Acid Metabolism ◽  
Indole Alkaloid ◽  
Tryptophan Decarboxylase ◽  
Decarboxylase Activity ◽  
Indole Compounds ◽  
Free Tryptophan ◽  
Potential Precursor

In barley seedlings, tryptophan is the precursor of the simple indole alkaloid gramine, and also of tryptamine, which is important as a potential precursor of the plant growth hormone 3-indoleacetic acid. The present investigation was designed to study the distribution of free tryptophan and its derivatives within the seedlings, and to follow the changes in these compounds with time. Development of the enzyme tryptophan decarboxylase, which catalyzes the conversion of tryptophan to tryptamine, was also studied. An increase in free tryptophan was detected within 2 h of soaking the seed; this compound reached high values in very young tissues, and then declined. Gramine and its precursors, 3-aminomethylindole and N-methyl-3-aminomethylindole, were confined to the shoots; all three compounds appeared together at the inception of shoot growth. Quantitatively, gramine was the most important compound present and reached a concentration of 623 μg/g fresh weight (25 times that of free tryptophan) on the 9th day, and then declined. Isolated embryos were capable of synthesizing gramine at about one quarter the normal rate, indicating that these embryos have a considerable inherent capacity for tryptophan synthesis and are not wholly dependent on tryptophan released by the endosperm. Tryptophan decarboxylase and tryptamine were found only in the shoot, and both enzyme and product appeared after the 1st week of growth, when the rate of gramine synthesis was beginning to decline. 5-Hydroxytryptamine began to accumulate in both shoot and root after about 2 weeks of growth, and N-methyl-5-hydroxytryptamine was also present in the roots. The close parallel between the gramine pathway of the barley shoot and the analagous hordenine pathway of the root, in which tyrosine is the precursor amino acid, is discussed.

4-(Tetrazolylalkyl)piperidine-2-carboxylic acids. Potent and selective N-methyl-D-aspartic acid receptor antagonists with a short duration of action

1991 ◽  
Vol 34 (1) ◽  
pp. 90-97 ◽  
Author(s):  
Paul L. Ornstein ◽  
Darryle D. Schoepp ◽  
M. Brian Arnold ◽  
J. David Leander ◽  
David Lodge ◽  
...  
Keyword(s):  
Aspartic Acid ◽  
Carboxylic Acids ◽  
Short Duration ◽  
Receptor Antagonists ◽  
Duration Of Action ◽  
Acid Receptor

Amino acid content of chronic undercut cortex of the cat in reletion to electrical afterdisctrarge: comparison with cobalt epileptogenic lesions

1977 ◽  
Vol 55 (3) ◽  
pp. 523-536 ◽  
Author(s):  
I. Koyama ◽  
H. Jasper
Keyword(s):  
Cerebral Cortex ◽  
Electrical Stimulation ◽  
Amino Acid ◽  
Glutamic Acid ◽  
Aspartic Acid ◽  
Amino Acid Metabolism ◽  
Acid Metabolism ◽  
Amino Acid Content ◽  
Opposite Hemisphere ◽  
Afterdischarge Threshold

Chronic undercutting of cerebral cortex in the cat for survival periods of 9 to 308 days was found to cause an increase in duration of epileptiform electrical, afterdischarge and a significant decrease in content of glutamic acid, GABA, and aspartic acid as compared with homologous cortex of opposite hemisphere. These changes were comparable (though less marked) with changes previously found in cobalt-induced experimental epileptogenic lesions. Rate of release of GABA, glutamic acid, and aspartic acid into superfusates of undercut cortex at rest was higher in undercut cortex and was increased further by electrical stimulation. It was concluded that chronic partial denervation of cerebral cortex causes prolonged changes in metabolism or storage of glutamic acid, GABA, and aspartic acid probably related to increased tendency to prolonged epileptiform discharge similar in some respects (though not all) to changes observed in cobalt-induced cortical epileptogenic lesions. However, electrical afterdischarge threshold was not reduced in chronically undercut cortex and prolonged afterdischarge was not necessarily related to concentration of GABA in superfusate from undercut cortex, suggesting that factors other than amino acid metabolism may be also involved in mechanisms of epileptogenesis in undercut cortex.

scholarly journals Transgenic Tobacco Plants Coexpressing the Agrobacterium tumefaciens iaaM and iaaH Genes Display Altered Growth and Indoleacetic Acid Metabolism

1992 ◽  
Vol 99 (3) ◽  
pp. 1062-1069 ◽  
Author(s):  
Folke Sitbon ◽  
Stéphane Hennion ◽  
Björn Sundberg ◽  
C. H. Anthony Little ◽  
Olof Olsson ◽  
...  
Keyword(s):  
Agrobacterium Tumefaciens ◽  
Transgenic Tobacco ◽  
Indoleacetic Acid ◽  
Acid Metabolism ◽  
Transgenic Tobacco Plants ◽  
Tobacco Plants

STUDIES ON INDOLEACETIC ACID METABOLISM: I. THE EFFECT OF METHYL UMBELLIFERONE, MALEIC HYDRAZIDE, AND 2,4-D ON INDOLEACETIC ACID OXIDATION

1953 ◽  
Vol 31 (4) ◽  
pp. 426-437 ◽  
Author(s):  
W. A. Andreae ◽  
Shirley R. Andreae
Keyword(s):  
Hydrogen Peroxide ◽  
Indoleacetic Acid ◽  
Acid Metabolism ◽  
Maleic Hydrazide ◽  
Acid Oxidation ◽  
Coumarin Derivatives ◽  
Stimulatory Action

Evidence is presented that IAA is oxidized with the liberation of hydrogen peroxide, and that the rate of oxidation is limited by a light-activated step. Methyl umbelliferone, maleic hydrazide, and 2,4-D stimulate IAA oxidation, presumably by accelerating the light-activated step. The stimulatory action of all three substances is overcome to a greater or less extent by scopoletin, which competitively inhibits the oxidation of IAA. It is suggested that maleic hydrazide and methyl umbelliferone may inhibit growth by causing an excessive oxidation of IAA. The importance of fluorescent coumarin derivatives on the photooxidation of IAA in vivo is discussed.

UPTAKE AND METABOLISM OF INDOLEACETIC ACID, NAPHTHALENEACETIC ACID, AND 2,4-DICHLOROPHENOXYACETIC ACID BY PEA ROOT SEGMENTS IN RELATION TO GROWTH INHIBITION DURING AND AFTER AUXIN APPLICATION

1967 ◽  
Vol 45 (5) ◽  
pp. 737-753 ◽  
Author(s):  
W. A. Andreae
Keyword(s):  
Growth Inhibition ◽  
Aspartic Acid ◽  
Indoleacetic Acid ◽  
Similar Degree ◽  
Dichlorophenoxyacetic Acid ◽  
Naphthaleneacetic Acid ◽  
Root Segments ◽  
Pea Root ◽  
2,4 Dichlorophenoxyacetic Acid ◽  
A Site

Growth inhibition by applied indoleacetic acid (IAA), naphthaleneacetic acid (NAA), or 2,4-dichlorophenoxyacetic acid (2,4-D) was studied using change in fresh weight of pea root segments as the criterion of growth. Auxin metabolism of these tissues was investigated with 14C-labeled auxins applied under conditions similar to those used in the growth studies.Growth inhibition by applied auxins is independent of the rate of auxin uptake, accumulation of auxin or auxin metabolites in the tissues, or the subsequent loss of accumulated auxin from the tissues. It is also independent of the metabolic processes leading either to auxin conjugation with aspartic acid or to decarboxylation. All three auxins inhibit growth to a similar degree, which depends only on the concentration of auxin applied and the pH of the solution. Inhibition persists undiminished as long as the auxin is applied. It is suggested that growth inhibition by applied auxin occurs at a site external to the cytoplasm, i.e. the cell wall or the cytoplasmic membrane.Growth inhibition of tissues after auxin treatment has ceased is not due to the auxin remaining in the tissues but rather to the auxin released from the tissues to the solution to which they have been transferred. Untreated tissues incubated in the same transfer solution with treated tissues are equally inhibited. The persistence of growth inhibition after treatment depends upon the ability of the tissues to convert accumulated auxins to physiologically inactive metabolites. Conjugation with aspartic acid accounts for the inactivation of all the accumulated NAA metabolized and the major part of the IAA. IAA decarboxylation under these conditions plays a lesser role. Growth recovery following treatment with IAA or NAA occurs as these auxins are metabolized. 2,4-D is not metabolized to any appreciable extent during these studies, and tissues remain inhibited to a degree consistent with the concentration of 2,4-D in the transfer solution.

Sign in / Sign up

Export Citation Format

Share Document