Decarboxylation Of Indoleacetic Acid Research Articles

Chilling-induced leaf abscission ofIxora coccineaplants. II. Alteration of auxin economy by oxidative stress

Chilling-induced leaf abscission of ixora (Ixora coccinea) plants was almost completely inhibited by α-naphthaleneacetic acid (NAA), even in the presence of exogenous ethylene, which enhanced the chilling effect on leaf abscission. Chilling reduced free indoleacetic acid (IAA) content, quantified immediately after chilling, in the abscission zone (AZ) and leaf blade. Free IAA content in chilling-treated plants continued to decrease gradually with time after chilling. Application of the antioxidant butylated hydroxyanisole (BHA) before or after chilling not only prevented the post-chilling decline in free IAA content, but also restored free IAA level during 6–48 h of the post-chilling period almost to the control level. No significant effect of chilling on the endogenous content of ester- and amide-conjugates of IAA or the metabolism of exogenous labeled IAA were observed. Chilling enhanced the decarboxylation of IAA, particularly in the AZ tissue. Auxin transport capacity was significantly inhibited by chilling, and this effect was counteracted by BHA applied before chilling. The data indicate that chilling reduces free IAA content in the AZ, an effect that may lead to increased sensitivity to ethylene. The chilling-induced reduction in IAA content in the AZ seems to result, at least in part, from increased IAA decarboxylation and reduced auxin transport capacity. These processes seem to be triggered by the oxidative stress imposed on the tissues by chilling.

Production of Skatole and para -Cresol by a Rumen Lactobacillus sp

The objective of this study was to examine the substrate specificity of several ruminal strains of a Lactobacillus sp. which previously was shown to produce skatole (3-methylindole) by the decarboxylation of indoleacetic acid. A total of 13 compounds were tested for decarboxylase activity. The Lactobacillus strains produced p-cresol (4-methylphenol) by the decarboxylation of p-hydroxyphenylacetic acid, but did not produce either o-cresol or m-cresol from the corresponding hydroxyphenylacetic acid isomers. These strains also decarboxylated 5-hydroxyindoleacetic acid to 5-hydroxyskatole and 3,4-dihydroxyphenylacetic acid to methylcatechol. Skatole and p-cresol were produced in a 0.5:1 ratio, when indoleacetic acid and p-hydroxyphenylacetic acid were combined in equimolar concentrations. Competition studies with indoleacetic acid and p-hydroxyphenylacetic acid suggested that two different decarboxylating enzymes are involved in the production of skatole and p-cresol by these strains. This is the first demonstration of both skatole production and p-cresol production by a single bacterium.

Transfer RNA-Peroxidase Interaction

Transfer RNA from wheat germ, yeast, and Escherichia coli inhibited the indoleacetic acid (IAA)-induced spectral change in horseradish peroxidase (EC 1.11.1.7) and the decarboxylation of IAA. The inhibition was limited to a delay after which the increase in A(427) and the decarboxylation of IAA resumed at the same rate as in the control; the duration of the inhibition was dependent on, but not proportional to, the concentration of tRNA. Alkaline hydrolysis destroyed the inhibitory activity of tRNA. The inhibition was completely abolished when the tRNA was added 30 seconds after IAA. Thus, the tRNA appears not to react with the enzyme intermediates formed during the reaction with IAA. The inhibition by tRNA was rapidly reversed by H(2)O(2) or additional IAA, but not by 2,4-dichlorophenol. Results suggest that the tRNA interferes with the initial reaction between IAA and the heme moiety of free peroxidase, thus preventing the formation of highly active enzyme intermediates essential for IAA degradation.

Inhibition of ruminal degradation of L-tryptophan to 3-methylindole, in vitro.

Available evidence supports the view that acute bovine pulmonary edema and emphysema (ABPE) is related to ruminal production of 3-methylindole (3MI) from L-tryptophan (TRP). Ruminal production of 3MI is a two-step process involving the conversion of TRP to indoleacetic acid (IAA) followed by decarboxylation of IAA and 3MI. Reduction in ruminal 2MI production by the inhibition of either of these processes may prevent the onset of ABPE. A closed-system, in vitro ruminal fermentation technique was used to screen 27 compounds for their ability to reduce the conversion of TRP to 3MI. Several compounds tended to reduce 3MI production at both 25 and 5 micrograms/ml. Desoxysalinomycin, X-206, chloral hydrate, nigericin, lasalocid, monensin, narasin and salinomycin all reduced 3MI production by more than 80% at 5 micrograms/ml without reducing total VFA production. All of these compounds, except chloral hydrate, are polyether antibiotics. At least part of the inhibition due to monensin and narasin occurs at the level of TRP conversion to IAA.

Abnormal Stomatal Behavior and Hormonal Imbalance in flacca, a Wilty Mutant of Tomato

The wilty tomato mutant flacca, the normal cultivar Lycopersicon esculentum Mill. Rheinlands Ruhm, and abscisic acid-induced phenotypic revertants were compared with respect to ethylene evolution, activity of tryptophan aminotransferase, and [1-(14)C]indoleacetic acid decarboxylation.The level of ethylene evolution was higher in flacca plants than in the normal cultivar. Ethylene evolution was reduced to the wild type level in abscisic acid-induced phenotypic revertants and to a lesser extent in mutant plants grown under humid conditions. Leaf epinasty, which characterized flacca plants in the present experiments, did not appear in absciscic acid-treated mutant plants, but did appear under high humidity. Tryptophan aminotransferase activity, similar to ethylene evolution, was higher in flacca plants and was reduced to the normal level by abscisic acid treatment. Indoleacetic acid decarboxylation was similar in mutant and normal plants, but was increased by abscisic acid treatment. The relationships among ethylene, auxin, and the morphological symptoms which characterize the mutant are discussed.

Metabolism of Indole-3-Acetic Acid

An indoleacetic acid oxidase preparation from an acetone powder of Parthenocissus tricuspidata crown-gall tissue has been examined. An intermediate in the reaction is 3-hydroxymethyloxindole and nonenzymic conversion of it to 3-methyleneoxindole was observed. Neither reaction mixtures nor 3-methyleneoxindole have any auxin-like activity in Avena or wheat coleoptile bioassays. In vivo studies show that although 53% decarboxylation of indoleacetic acid was observed in 48 hours, only a small amount of 3-methyloxindole could be recovered from the medium. The other decarboxylated products remain to be identified but are not 3-hydroxymethyloxindole or 3-methyleneoxindole.

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

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.