Search

Higher plants are commonly exposed to rapid changes in the amounts and proportions of ammonium and nitrate in their root environment. Some of the potential consequences of such changes have been determined by examining the suppressive effects of growing maize (Zea mays L.) seedlings with a high concentration (3 mM) of nitrogen on the subsequent uptake of nitrogen from a more dilute (0.2 mM) solution. To document the interactive role of nitrate and ammonium supply in suppression, ratios of these ions in the growth solution were maintained at 3:0, 2:1, 1:2 and 0:3. Rates of nitrate and ammonium uptake were then measured during initial (0-1 h) exposure to 0.2 mM KNO3 or NH4NO3 and hourly during a subsequent 7 h period of adaptation to the dilute solutions. Maximal suppression of nitrate uptake occurred only when both nitrate and ammonium were present (2:1 and 1:2) during prior growth. Nitrate uptake rates increased two- to three-fold as the seedlings adapted to the dilute KNO3 solution, but the presence of ammonium with nitrate in the prior growth solution restricted the rate and extent of recovery from suppression. Recovery was further restricted when ambient ammonium was present during the adaptation period. Neither the magnitude of suppression nor the rate and extent of recovery was readily explained by (a) the proportion of nitrate and ammonium present during prior growth, (b) carbohydrate concentrations in root and shoot tissues, (c) concentrations of nitrate and ammonium in the root tissue, or (d) indirect effects of ammonium on potassium uptake. Total nitrate reduction by the entire plant in the 8 h adaptation period decreased as the proportion of ammonium in the prior growth solution increased. Ambient ammonium restricted nitrate reduction only in seedlings previously grown entirely with ammonium. Thus the effect of ambient ammonium on nitrate reduction by the whole plant differed substantially from that on nitrate uptake. Since nearly all the ammonium taken up by the roots was assimilated, as well as that generated by nitrate reduction, it appears that carbohydrate supply did not limit the observed uptake of ammonium and nitrate. The accumulation in roots of both nitrate and specific metabolites of ammonium serving as negative effectors could account for most of the observations. [ABSTRACT FROM AUTHOR]

Two-week-old nitrogen-deficient wheat plants attained a high rate of nitrate uptake on the first day of exposure to nutrient solutions supplemented with KNO3. Ammonium uptake from similar solutions supplemented with NH4NO3 was also high during the first day of exposure, but nitrate uptake from this solution was lower than from the KNO3 treatment. During the next two to three days there was a progressive decrease in uptake of both nitrogen ions. A steady increase in uptake then occurred as the plants fully recovered from the nitrogen deficient state. The transient low nitrate uptake after three or four days of exposure to KNO3 was not due to an excessive accumulation of nitrate in the tissue, nor to a failure in nitrate reduction as indicated by the rate of nitrate accumulation relative to the uptake rate. Nitrogen supplied as 15N-nitrite during the low uptake period was effectively incorporated into organic forms and effectively translocated to the shoots Failure of the root tissue to increase in soluble carbohydrates during illumination was characteristic of the low uptake period. This contrasted with an increase in root soluble carbohydrates in the light during rapid uptake associated with full recovery from the nitrogen-deficient state. It is concluded that carbohydrate translocation to the root system was insufficient during the intermediate recovery period fot optimal nitrate uptake, although it was sufficient for effective reduction and translocation of nitrate and reduced nitrogen. Ammonium uptake from NH4NO3 was restricted during darkness by the third day whereas there was little difference between light and dark periods in nitrate uptake from KNO3 until about the sixth day of recovery. The extent to which ammonium restricted nitrate uptake increased progressively for two or three days following which a lessening influence seemed evident, and the effects were not directly associated with the rate of ammonium uptake. [ABSTRACT FROM AUTHOR]

Intact, 14‐day‐old nitrogen‐depleted wheat (Triticum vulgare cv. Blueboy) seedlings were exposed to solutions of 0.5 mM KNO2, 0.05 mM CaSO4 and 1 mM sodium 2‐[N‐morpholino]‐ethanesulfonate, pH 6.1. Nitrite uptake was determined from depletion of the ambient solution or from incorporation of 15N in the tissue. An initial nitrite uptake shoulder was followed by a relatively slow uptake rate which subsequently increased to a substantially greater rate. This accelerated phase was maintained through 24 h. Nitrite accumulated to a slight extent in the root tissues during the first few hours but declined to low values when the accelerated rate was fully developed, indicating an increase in nitrite reductase activity paralleling the increase in nitrite uptake capacity. About 50% of the nitrogen absorbed as nitrite was translocated to the shoots by 9–12 h. Development of the accelerated nitrite uptake rate was restricted in excised roots, in intact plants kept in darkness, by 400 μg puromycin ml−1 and by 1 mM L‐ethionine. When puromycin and L‐ethionine were added after the accelerated phase had been initiated, their effects were not as detrimental as when they were added at first exposure to KNO2. The two inhibitors restricted translocation more than uptake. The data indicate an involvement of protein synthesis and a requirement for movement of a substance from shoots to roots for maximal development of the accelerated nitrite uptake phase. A requirement for protein synthesis in the transport of soluble organic nitrogen from roots to shoots is also suggested. [ABSTRACT FROM AUTHOR]

Potassium (86Rb) influx from 200mmol m-3 KCl into dark grown, decapitated maize seedlings 6 d old) was stimulated by nitrate pretreatment. The stimulus was clearly evident by 6h exposure to nitrate and required 12-24 h for maximal expression. Decay of the nitrate-stimulated potassium influx was more than 50% complete within 3 h after transfer to nitrogen-free solutions. The stimulation of potassium influx was entirely accounted for by an increase in the influx component that was resistant to inhibition by presence of 200 mmol m-3 ambient ammonium. In contrast, the component of potassium influx that was sensitive to inhibition by ambient ammonium was unaffected by nitrate pretreatment. Exposure to the glutamine synthetase inhibitor L-methionine-dl-sulphoximine (MSX) during nitrate pretreatment stimulated the resistant component but the sensitive component was nearly eliminated. Pretreatment with ammonium increased the resistant component of potassium influx within 3 h, i.e. before it was increased by nitrate pretreatment, but the sensitive component was concomitantly restricted. The latter recovered partially during extended pretreatment with ammonium. The data indicate that the resistant component responded positively to increases in tissue ammonium concentrations whereas the sensitive component was unaffected by tissue ammonium except at concentrations in excess of 10 μmol g-1. Ammonium influx was also stimulated by nitrate pretreatment and to a greater extent than potassium influx. Presence of MSX with nitrate during pretreatment resulted in a further stimulation in ammonium influx. The parallel increases in root ammonium concentrations with the two pretreatments imply that part of the increase in ammonium influx was a consequnce of increased countertransport with endogenous ammonium. [ABSTRACT FROM AUTHOR]