Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008272 (chlorosis)
 2,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The specificity of the Pseudomonas phaseolicola toxin for enzyme inhibition and its relationship to toxin-induced chlorosis in bean leaves (Phaseolus vulgaris L.) was examined. The toxin showed no significant inhibitory activity against glutamine synthetase, glutamine transferase, carbamyl phosphate synthetase, aspartate carbamoyltransferase, or arginase at concentrations 100-fold higher than that needed to inhibit ornithine carbamoyltransferase by 50%.Protection from and reversal of toxin-induced chlorosis in bean leaves was attempted with several amino acids. Aside from protection with l-citrulline which was previously reported, only l-arginine-HCl and to a minor extent l-leucine and l-glutamine showed protection from chlorosis. l-Citrulline and l-arginine-HCl (but not l-glutamine and l-leucine) also reversed toxin-induced chlorosis.Ultrastructurally, cells from toxin-treated chlorotic tissues showed no observable changes as compared to nontreated tissues. This, together with the ability of the two amino acids to reverse chlorosis, indicated that the toxin causes a reversible biochemical lesion in treated tissue.While tissues from bean plants inoculated with P. phaseolicola showed a large accumulation of ornithine, toxin-treated tissues showed no accumulation of ornithine. The latter finding indicated that in addition to the ornithine carbamoyltransferase inhibitor, the pathogen may produce inhibitors of other ornithine metabolizing enzymes in inoculated tissues.
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PMID:Mode of Action of the Toxin from Pseudomonas phaseolicola: I. Toxin Specificity, Chlorosis, and Ornithine Accumulation. 1665 52

A chlorosis-inducing toxin of Pseudomonas phaseolicola was examined for inhibition of ornithine carbamoyltransferease prepared from acetone powder of bean (Phaseolus vulgaris L.) plants. The enzyme has a pH optimum at 8.5, involves a ternary complex reaction mechanism, and shows Michaelis constants of 5.0 mm and 1.7 mm for ornithine and carbamoylphosphate, respectively. Assuming reversible catalysis, Michaelas constants of 11 mm and 3.3 mm are calculated for citrulline and arsenate. Toxin induces allosteric competitive inhibition in relation to carbamoylphosphate and a noncompetitive mode of inhibition in relation to ornithine, except at high toxin concentrations where uncompetitive inhibition is observed. In the backward assay, competitive inhibition is observed for both arsenate and citrulline. Inhibition is increased with preincubation time and shows saturation kinetics with regard to toxin concentration.
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PMID:Mode of Action of the Toxin from Pseudomonas phaseolicola: II. Mechanism of Inhibition of Bean Ornithine Carbamoyltransferase. 1665 53

Phaseolotoxin ([N(delta)-phosphosulfamyl]ornithylalanylhomoarginine) is produced by Pseudomonas phaseolicola (Burkh.) Dows. in liquid culture. When phaseolotoxin was applied to leaves of bean (Phaseolus vulgaris L.) at 0.1 to 1 nmoles/g fresh weight of leaf by a prick-assay procedure, the characteristic "halo" symptom of bean halo blight disease developed after 24 to 48 hours. At higher concentrations (10-100 nmoles/g fresh weight) the systemic symptoms, which are commonly a feature of diseased plants, also developed after 24 to 48 hours.When applied to bean leaves, phaseolotoxin was rapidly broken down by the sequential removal of homoarginine and alanine. N(delta)-Phosphosulfamylornithine was the major product formed, although phosphosulfamate and unreacted phaseolotoxin were also present. When P. phaseolicola infected bean plants, very little phaseolotoxin was detected within the plant, but the amount of N(delta)-phosphosulfamylornithine formed was sufficient to account for the observed chlorosis, the ornithine accumulation, and the systemic symptoms. N(delta)-Phosphosulfamylornithine therefore seemed to be the main functional phytotoxin of bean halo blight disease.When (35)S-phaseolotoxin was applied to primary leaves, (35)S (assumed to be a mixture of phaseolotoxin, N(delta)-phosphosulfamylornithine, and phosphosulfamate) was actively loaded into the fine veins of the leaf and moved through the plant in the vascular system at a speed greater than 3 cm/hour, particularly toward the apical and lateral buds and the root tips. Certain factors which affect pholem transport (arsenate, cold) affected toxin movement and the expression of systemic symptoms. Autoradiography suggested that the (35)S was transported in the phloem.A model for the involvement of phaseolotoxin in halo blight disease is presented.
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PMID:Involvement of phaseolotoxin in halo blight of beans: transport and conversion to functional toxin. 1666 Jan 72

The chlorosis symptom that characterizes the halo blight disease of Phaseolus vulgaris L. is caused by phaseolotoxin produced by the plant pathogenic bacterium Pseudomonas syringae pv phaseolicola. Phaseolotoxin is hydrolyzed by plant peptidases to N(delta)(N'-sulpho-diaminophosphinyl) -l-ornithine which also causes chlorosis and is reported to be an irreversible inhibitor of ornithine carbamoyltransferase (OCTase). We have examined the hypothesis that inhibition of OCTase is the primary action of phaseolotoxin that leads to chlorosis.Chlorotic spots appeared on the primary leaves of P. vulgaris seedlings during the 2 days following leaf prick application of a minimum of 30 picomole phaseolotoxin. OCTase in extracts of the lesions was reduced to 20%, or less, of the activity in controls. Four hours after the application of phaseolotoxin the concentration of free ornithine increased more than 2-fold. Other amino acids, especially glutamine and asparagine-but not arginine-increased later. Chlorophyll remained at a constant level in the phaseolotoxin-treated tissue and the appearance of chlorosis was due to the increase in chlorophyll in the surrounding unaffected tissue.Clear halo symptoms developed only on primary leaves of the youngest seedlings (treated 6-7 days after germination). Lesions did not develop on primary leaves of seedlings more than 14 days old, in which the chlorophyll concentration had reached a maximum. OCTase also was inhibited in the symptomless tissue from older leaves treated with phaseolotoxin, but there was no accumulation of amino acids, including ornithine. A single appliction of 200 nanomoles arginine resulted in the complete regreening of the chlorosis caused by phaseolotoxin. Soluble protein was lower in the chlorotic tissue than in the controls, but increased to greater than the control value following the appliction of arginine. These results suggest that phaseolotoxin-induced chlorosis results from reduced chlorophyll synthesis that is associated with arginine-starvation in the tissue where OCTase is inhibited.
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PMID:Association between Symptom Development and Inhibition of Ornithine Carbamoyltransferase in Bean Leaves Treated with Phaseolotoxin. 1666 33

Mesophyll cells in discs cut from primary leaves of Phaseolus vulgaris L. were exposed to a concentration of phaseolotoxin that inhibited ornithine carbamoyltransferase (OCTase) measured in an extract of the tissue. This treatment also blocked incorporation of exogenous [(14)C] ornithine into protein-arginine of the mesophyll cells. By contrast more than 80% of the [(14)C]ornithine supplied to untreated tissue was incorporated into protein-arginine in 565 minutes. Protein synthesis in mesophyll cells was unaffected by phaseolotoxin because treated tissue continued to incorporate [(14)C]leucine into protein at the same rate as the untreated control. The phaseolotoxin-treated tissue should therefore remain metabolically competent and this prediction was reinforced by the finding that the rate of photosynthetic O(2) evolution per unit chlorophyll was similar for tissue from the phaseolotoxin-induced chlorosis and from green healthy tissue. Phaseolotoxin also blocked OCTase but not protein synthesis in exponentially growing cell suspension cultures. Phaseolotoxin rapidly inhibited growth of Escherichia coli and this effect was rapidly reversed by arginine. Thus, the toxic effects of phaseolotoxin may be attributed to the inhibition of OCTase which, in turn, blocks arginine synthesis. Protein accumulation is blocked as a consequence, but protein synthesis is unaffected. Chlorosis is due to reduced chlorophyll synthesis and this is presumably a consequence of the lower protein level in affected tissue.
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PMID:Effect of phaseolotoxin on the synthesis of arginine and protein. 1666 98

We focused on the changes of metabolite profiles in navel orange plants under long-term boron (B) deficiency using a gas chromatography-mass spectrometry (GC-MS) approach. Curling of the leaves and leaf chlorosis were observed only in the upper leaves (present before start of the treatment) of B-deficient plants, while the lower leaves (grown during treatment) did not show any visible symptoms. The metabolites with up-accumulation in B-deficient leaves were mainly proline, l-ornithine, lysine, glucoheptonic acid, fucose, fumarate, oxalate, quinate, myo-inositol and allo-inositol, while the metabolites with down-accumulation in B-deficient leaves were mainly serine, asparagine, saccharic acid, citrate, succinate, shikimate and phytol. The levels of glucose and fructose were increased only in the upper leaves by B deficiency, while starch content was increased in all the leaves and in roots. The increased levels of malate, ribitol, gluconic acid and glyceric acid occurred only in the lower leaves of B-deficient plants. The increased levels of phenols only in the upper leaves indicated that the effects of B on phenol metabolism in citrus plants may be a consequence of disruptions in leaf structure. Metabolites with opposite reactions in upper and lower leaves were mainly glutamine, glycine and pyrrole-2-carboxylic acid. To our knowledge, the phenomena of allo-inositol even higher than myo-inositol occurred characterized for the first time in this species. These results suggested that the altered pattern of central metabolism may be either specific or adaptive responses of navel orange plants to B deficiency.
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PMID:Metabolic profiling reveals altered pattern of central metabolism in navel orange plants as a result of boron deficiency. 2521 59