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1. The growth of Avena coleoptile sections in sucrose and auxin solutions is inhibited by various substances which are known to act as dehydrogenase inhibitors. 2. Iodoacetate, which is particularly active in this connection, inhibits all growth at a concentration of 5 x 10–5 M, but produces only a slight inhibition of oxygen uptake. 3. The growth inhibition by iodoacetate is completely removed by malate and fumarate, and to a lesser extent by succinate and pyruvate. 4. These acids themselves increase the effect of auxin on growth and also increase the respiration of the coleoptile sections, but only if auxin is present. 5. When sections have been soaked in malate or fumarate, the addition of auxin considerably increases the total respiration. Further, the concentration range over which this increase takes place parallels that active in promoting growth. 6. The four-carbon acids provide a respiratory system which is part of the chain of growth processes, and which is in some way catalyzed by auxin. It represents a small but variable fraction of the total respiration.  相似文献   

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Intracellular localization of the native auxin in the Avenacole-optile tip was investigated by separating cellular fractionsby differential centrifugation. Each fraction was extractedwith ether and the auxin activity was measured by the sensitizedAvena curvature test. After the removal of the native free auxin,each fraction was alkaline-hydrolyied, and from these hydrolyzatesthe bound auxin was extracted with ether and its activity wasmeasured. Both the native free auxin and the native bound auxinin these extracts were identified as IAA by paper chromatography.The results show that the native free auxin occurs only in thesupernatant soluble cytoplasm, and that the native bound auxinlocalizes also in the supernatant. The distribution of the externallyapplied IAA was also investigated. (Received February 27, 1962; )  相似文献   

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Effect of yeast (Saccharomyces cerevisiae) sexual hormones on the elongation of etiolated Avena coleoptile segments was studied. The elongation was promoted by a hormone excreted by cells of mating type a, but not by α hormone excreted by cells of α type. The effect of the former was as great as that of 5 mg/1 indole-3-acetic acid in the first hour of application. The optimal concentration of a hormone was 10 units/ml. Its growth promoting effect was greatly inhibited by an antiauxin, 2,4,6-trichlorophenoxyacetic acid. a Hormone increased cell wall extensibility just as auxin does. Testosterone, β-estradiol, progesterone and ergosterol showed very little effect on the elongation of coleoptile segments.  相似文献   

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  1. Previous reports that Michaelis enzyme kinetics may be appliedto the system controlling cell elongation in Avena coleoptilesare confirmed.
  2. Substrate (applied hormone) and enzyme arenot in direct contactwith each other. Active transport of theapplied hormone incoleoptile sections, and permeability ofcells to hormone, regulatethe intracellular substrate concentration,thereby markedlyinfluencing the value of K5, a parameter givinga measure ofthe affinity of substrate for enzyme.
  3. The effectof permeability and transport factors on calculatingK1 valuesof competitive hormone inhibitors is considered. Dataof otherworkers are used to show that observed K1 values arenot necessarilyindependent of the hormone used.
  4. Auxin-induced inhibitionof cell elongation results primarilyfrom a toxic action ofhormones on cell protoplasm leading finallyto cellular disorganization,shrinkage, and death. The datado not decisively support thehypothesis of inhibition resultingfrom steric hindrance totwo-point attachment between substrateand enzyme.
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