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Kinetin in concentrations of 10(-8) to 10(-4)m, stimulated ethylene production in 3 and 4-day old etiolated seedlings of Alaska pea (Pisum sativum L. var. Alaska). Seedlings of other species responded similarly. The response to kinetin depended on the age of the seedlings.Kinetin alone did not influence ethylene production in 6-day old stem sections, but it greatly increased the enhancing effect of IAA.Gibberellic acid had no effect on ethylene production by pea seedlings during the first 6 days of growth. Ethylene and gibberellic acid are antagonistic in their effects on growth of the seedlings; ethylene interfered severely with the action of gibberellic acid but did not completely suppress it.The inhibitors cycloheximide, cupferron, and N-ethylmaleimide, caused considerable inhibition of kinetin-induced ethylene production but were much less effective in the endogenous ethylene-forming system.
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Auxin-induced elongation and cell wall polysaccharide metabolism were studied in excised hypocotyl sections of ponderosa pine (Pinus ponderosa) seedlings. Sections excised from hypocotyls of ponderosa pine elongate in response to the addition of auxin. The neutral sugar composition of the extracellular solution removed from hypocotyl sections by centrifugation was examined. In cell wall solution from freshly excised sections, glucose, galactose, xylose, and arabinose make up more than 90% of the neutral sugars, while rhamnose, fucose, and mannose are relatively minor components. The neutral sugar composition of the polysaccharides of the pine cell wall solution is both qualitatively and quantitatively similar to that of pea. Following auxin treatment of pine hypocotyls, the neutral sugar composition of the cell wall changes; glucose, xylose, rhamnose, and fucose increase by nearly 2-fold relative to controls in buffer without auxin. These changes in neutral sugars in response to auxin treatment are similar to those found in pea, with the exception that in pea, rhamnose levels decline in response to auxin treatment.
Evidence for the occurrence of indole 3-acetic acid in Caulerpa paspaloides extracts was obtained by bioassay, by high-performance liquid chromatography with an electrochemical detector, and by capillary gas chromatography combined with mass spectrometry. The amount of indole 3-acetic acid present was estimated to be about 1 milligram per kilogram fresh weight, with an error limit of one order of magnitude. This is in the range reported from angiosperms.
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A high resolution growth measuring apparatus was used to demonstrate the inhibition of auxin-induced cell elongation in oat coleoptile segments (Avena sativa L. var Holden) by lead at concentrations ranging from 2 x 10-6 M to 2 x 10-3 M. The inhibition was immediate, having no measurable lag period. Electron micrographs of lead-treated and control segments revealed that in the treated material, lead became localized as electron-dense granules in the cell walls and in vesicles associated with dictyosomes. These granules were found to be lead hydroxide phosphate by electron diffraction techniques. The possible significance of this localization and identification with regard to phosphatase activity is discussed.
The dependence of growth induced by the fungal toxin fusicoccin (FC) on the K+ content of the incubation medium was investigated in abraded maize coleoptiles. If the divalent ion Ca2+ was included in the bathing medium, no FC-induced growth occurred in the absence of K+, whereas a strong response was detected in presence of K+. The optimal K+ concentration was in the range of 1-10 mM. With the exception of Rb+, none of the other alkali ions (Na+, Li+, Cs+) could replace for K+ in sustaining FC-induced growth. The potassium channel blocker tetraethylammonium (TEA) reversibly inhibited FC-induced growth. As shown earlier for auxin-induced growth, no strict potassium dependence of FC-triggered elongation was observed in Ca2+ -free media. However, TEA abolished this apparently K+ independent FC-induced growth. It is concluded that FC-induced growth, like auxin-induced growth, requires K+ uptake through K+ channels.
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