THE EFFECTS OF INDOLEACETIC ACID AND 2, 4-DICHLOROPHENOXYACETIC ACID ON INTERMEDIARY METABOLISM OF 14C-LABELLED ORGANIC ACIDS BY PEA ROOT TIPS

1967 ◽  
Vol 45 (10) ◽  
pp. 1789-1796 ◽  
Author(s):  
W. K. Kim ◽  
R. G. S. Bidwell

The effects of indoleacetic acid (IAA) and 2, 4-dichlorophenoxyacetic acid (2, 4-D) on the metabolism of 14C-specifically labelled pyruvic, acetic, succinic, and glutamic acids by pea root tips have been examined. The conversion of 14C from the substrates into alcohol-soluble and -insoluble fractions and respired CO2 was determined, and the radioactivity of certain soluble amino acids and organic acids was measured after chromatography. While pyruvic acid decarboxylation is unaffected, the carboxylation of pyruvic acid and the entry into the Krebs cycle of acetate derived from pyruvate is inhibited by the hormones. Acetate, however, is oxidized to CO2 much more rapidly in the presence of IAA or 2, 4-D. The accumulation of 14C in Krebs cycle intermediates or amino acids derived from them is prevented by the auxins. The results indicate that IAA and 2, 4-D have an inhibiting effect either on co-carboxylase or more likely on α-lipoic acid metabolism, but not on coenzyme A (CoA). Other specific effects on the metabolism of individual amino acids are also indicated.

1967 ◽  
Vol 45 (9) ◽  
pp. 1751-1760 ◽  
Author(s):  
W. K. Kim ◽  
R. G. S. Bidwell

The effect of indoleacetic acid and 2,4-dichlorophenoxyacetic acid on the uptake and metabolism of 14C-labelled glucose and amino acids by excised pea root tips was studied. The intention was to determine whether the observed reduction of root growth by growth hormones was caused by interference in the uptake or in the metabolism of compounds by roots. The results indicate that the main effect of auxins on sugar metabolism in root tips is not on uptake, but on the subsequent metabolism of glucose. Auxins also had several specific rather than general effects on the synthesis of proteins. The production of certain amino acids from glucose was prevented, and the entry of others into protein was affected. This indicates that effects of auxin on protein metabolism were specific, and not necessarily merely consequences of decreased rates of growth and metabolism.


2017 ◽  
Author(s):  
Rakesh Kumar ◽  
Vajir Tamboli ◽  
Rameshwar Sharma ◽  
Yellamaraju Sreelakshmi

AbstractSeveral Penjar accessions of tomato (Solanum lycopersicum), widely grown in the Mediterranean region, exhibit prolonged shelf life, and harbor alcobaca mutation with valine-106-aspartic acid substitution in the NAC-NOR protein. To uncover the metabolic basis underlying the prolonged shelf life, we compared four Penjar accessions to Ailsa Craig (AC). Three accessions bore alcobaca mutation, whereas fourth was a novel NAC-NOR allele with only six amino acids in the encoded protein. The cuticle composition among Penjars varied widely during the progression of fruit ripening. All Penjars exhibited delayed ripening, prolonged on-vine and off-vine shelf life, low ethylene emission and carotenoid levels albeit with accession-specific differences. Metabolic profiling revealed shifts in Krebs cycle intermediates, amino acids, and β-aminobutyric acid levels indicating the attenuation of respiration in Penjars during post-harvest storage. The prolonged shelf life of Penjar fruits was associated with a concerted downregulation of a number of cell-wall modifying genes and cell-wall-related metabolites. The accumulation of higher ABA and sucrose levels at the onset of senescence in Penjar fruits likely contribute to reduced water loss. Our analyses reveal that in addition to specialized cuticle composition, the attenuation of various metabolic processes by NAC-NOR mutation likely prolongs the shelf life of Penjar fruits.HighlightThe prolonged shelf life of tomato Penjar accessions bearing mutations in NAC-NOR transcription factor appears to be regulated by a combined effect of attenuation of respiration, altered cuticle composition, enhanced ABA and sucrose levels in fruits and downregulation of cell wall modification


1973 ◽  
Vol 52 (2) ◽  
pp. 171-173 ◽  
Author(s):  
David A. Steen ◽  
Arthur V. Chadwick

1975 ◽  
Vol 21 (9) ◽  
pp. 1369-1371
Author(s):  
Noel R. Funderburk ◽  
A. S. Kester

Fifteen isolates of Bacteroides were tested for their ability to dehydrogenate a variety of amino acids and organic acids. A simple and rapid method was developed for detecting dehydrogenase activity using 2,3,5-triphenyl tetrazolium chloride as a hydrogen acceptor and indicator. The results indicate that the tests for valine, malic, and pyruvic acid dehydrogenases have value in differentiating organisms in this genus.


1967 ◽  
Vol 45 (5) ◽  
pp. 737-753 ◽  
Author(s):  
W. A. Andreae

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.


1968 ◽  
Vol 46 (7) ◽  
pp. 945-947
Author(s):  
W. K. Kim ◽  
R. G. S. Bidwell

Hydrogen ion concentration has been found to have a marked effect on the response of pea root tips to auxins. In addition, auxins have been shown to exert certain specific effects on the metabolism of 14C-labelled glucose and related metabolites. The present experiments show that varying the pH modifies the auxin effects on intermediary metabolism and growth in entirely different ways. It is concluded that the auxin inhibition of growth must operate through a different mechanism than the effect on inter mediary metabolism of glucose.


1953 ◽  
Vol 140 (901) ◽  
pp. 522-555 ◽  

In part III of this series data were presented for the changes in air following periods of anaerobiosis in the rate of CO 2 production of potato tubers and in the contents of sugar, lactic acid and other constituents. Here these experimental data are analyzed and further discussed. The time curve for decrease in the content of lactic acid in air following a period of anaerobiosis appeared to be nearly linear initially with a sharp inflexion as the air value of lactic acid was approached. For a given content of lactic acid the rate of loss of the acid was the more rapid, the shorter the period of anaerobiosis. Preliminary data for the changes in the content of pyruvic and other keto-acids in air following nitrogen were mentioned and the forms of the curves for loss of lactic acid were considered in relation to the system pyruvic acid + Co I. H 2 ⇌ L-lactic acid + Co I lactic dehydrogenase The possible influence of changes both in the content of pyruvic acid and in the quotient Co I. H 2 /Co I on the form of the lactic acid content/time curve was noted. It was provisionally suggested that the effective activity of lactic acid dehydrogenase might decrease progressively in nitrogen and that this loss of activity might not be quickly reversed in air following nitrogen; alternatively in air following nitrogen, owing to the accumulation of reduced compounds during anaerobiosis, the quotient Co i.H 2 /Co i might for a time be maintained larger the longer the previous period of anaerobiosis. The CO 2 production in the after-effect was shown to have a dual origin, being derived partly from lactic acid and partly from sugar. The view was advanced that lactic acid was first oxidized to pyruvic acid, which was then transformed, either in part or completely, into other acids, possibly via the Krebs cycle. The keto-acids of the Krebs cycle may thus be the immediate substrates of the CO 2 production which is derived from lactic acid. The quantitative evaluation of the share of the two components, i. e. the non-sugar and the sugar CO 2 components, in the total CO 2 production, and the elucidation of the fate of the lactic acid presented serious difficulties. The analysis of the CO 2 production/sucrose relation during the after-effect in dicated that when lactic acid had decreased to the low level characteristic of aerobic conditions the CO 2 production was, for a time which varied in extent in the different experiments, approximately proportional to the sucrose concentration; how ever, in comparison with the values for samples held through out in air, the proportionality factor, i. e. CO 2 production/sucrose, was depressed to a greater or lesser extent in different experiments. If it was assumed first that the depression of sugar respiration during the time when lactic acid was disappearing was no greater than after the acid had decreased to the air-level and second that the respiration of sugar continued normally in the after-effect unaffected by the simultaneous oxidation of lactic acid, only a part of the lactic acid loss could be accounted for by CO 2 production; it was suggested that the residue of the lactic acid was either in part metabolized to other compounds, e. g. other organic acids, or was in part resynthesized to carbohydrate as in frog’s muscle (Meyerhof 1930). If, however, the respiration of sugar was assumed to be partly suppressed by the increased concentration of pyruvic acid arising from the rapid oxidation of lactic acid, then a greater proportion but not the whole of the lactic acid loss could be accounted for as CO 2 production; in this case, in addition to conversion to other organic acids and possibly resynthesis to carbohydrate as already mentioned, a part of the lactic acid would be oxidized in stead of sugar and so spare the normal consumption of sugar in respiration. The results confirm the observations of Singh (1927) on CO 2 production in the after-effect and extend them by the information provided by the data for the concomitant changes in the contents of lactic acid and sugar.


1970 ◽  
Vol 48 (11) ◽  
pp. 2001-2007 ◽  
Author(s):  
D. J. Mitchell ◽  
R. G. S. Bidwell

14C-Labeled aspartate and organic acids were supplied to pea-root pieces to elucidate the pathways of carbon leading to asparagine and homoserine synthesis. The pattern of labeling in the products, and the effects of competing non-radioactive acids on the distribution of 14C from labeled substrates, gave the following results. Supplied aspartate is not converted directly to asparagine or homoserine, but must first enter the Krebs cycle. If aspartate is an immediate precursor of either of these compounds, the synthetic pathways must be compartmented from externally supplied aspartate. Carbon leaves the Krebs cycle as succinate, and is converted to other 4-carbon acids in a metabolic system that is separated from the Krebs cycle and presumably outside the mitochondria. The pathway from succinate to homoserine proceeds via extramitochondrial fumarate and malate, and to asparagine via fumarate. Carboxylation of pyruvate (or a related three-carbon acid) leads to homoserine and asparagine via a symmetrical intermediate permitting equilibration of the two ends of the 4-carbon precursor. About four times more carbon from added pyruvate is converted to homoserine and asparagine via the Krebs cycle than by carboxylation.


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