Response of strawberry plants to manganese nutrition

Abstract

The effects of manganese nutrition on growth, mineral composition, carbohydrate and nitrogen metabolism, IAA oxidase and phenols of 'Northwest' strawberry plants are reported. Growth and mineral composition response were investigated in sand culture and Hoagland's solution 2 modified to contain 0.0, 0.5, 2.5, 12.5, 25.0, 62.5 and 125.0 ppm substrate manganese. The remaining aspects of the study were conducted using the Hoaglands solution in a hydroponics system with manganese levels of 0.0, 0.5, 2.5, 12.5 and 25.0 ppm in the nutrient solution. In sand culture, symptoms of manganese toxicity occurred first in old leaves after three weeks of 125.0 ppm Mn treatment; after five weeks at 62.5 ppm; and after 13 weeks at 25.0 ppm substrate Mn. Toxicity symptoms appeared as necrotic spots along the margins of leaves; these spots enlarged greatly within a few days and ultimately killed all the leaves. All the plants treated with 62.5 and 125.0 ppm Mn died within 7 and 11 weeks, respectively. Young leaves of runners from the plants treated with 0.0 ppm Mn developed interveinal chlorosis and cupping after 12 weeks. Later, these leaves developed chlorotic spots which expanded to chlorotic bands. Plant weight and total leaf area of the plants harvested after 20 weeks was greatest with 2.5 ppm Mn treatment, and decreased both at lower or higher substrate manganese. The most leaves and runners were produced at 25.0 ppm treatment; whereas area per leaf was highest at 0.5 ppm Mn. Manganese present in tissue was directly correlated to substrate manganese levels and was also related to the plant part. Accumulation of manganese occurred in all tissues at high substrate Mn levels, indicating that the tolerance of strawberry plants to high Mn is not because of low uptake but due to their ability to endure large amounts of accumulated Mn. In Mn deficient plants, the differences in the concentration of Mn in the various tissues were small, suggesting the possibility of redistribution of the element under conditions of deficiency. Highest levels of tissue iron were found in 0.0 ppm Mn treatment followed in order by 2.5, 0.5, 12.5 and 25.0 ppm substrate Mn. A strong inverse relationship was noted between the tissue iron/ manganese ratio and the substrate Mn. The deficiency and excess of Mn resulted in a decrease in the concentration of Mg and P in the leaves. Highest levels of these elements were observed with 2.5 ppm Mn treatment. The most vigorous plants were produced at 2.5 ppm Mn treatment when old and young leaves contained 955.7 and 617.4 ppm Mn, respectively. Typical toxicity symptoms were shown by plants when Mn in young leaves reached about 4,000 and in old leaves 9,000 ppm. In the hydroponic system, manganese deficiency and toxicity resulted in a decrease in sugar as well as starch content in the leaves, except in old leaves at 25.0 ppm Mn treatment which contained the highest levels of starch. Total and insoluble N increased whereas nitrate N decreased with the increase in substrate Mn. Lowest levels of soluble and soluble reduced N were found at 2.5 and 0.5 ppm Mn treatment, respectively. Both the excess and deficiency of Mn resulted in the accumulation of amino acids. The highest concentrations of nitrate and lowest concentrations of insoluble N observed in Mn deficient plants indicate that the Mn is not involved in nitrate N absorption but may be concerned in protein synthesis. High IAA oxidase activity was found in enzyme extracts of young and old leaves of deficient and toxic plants. Total and bound phenols, in general, were directly related to substrate manganese. Low levels of free phenols were found in conditions of excess and deficiency of Mn. The increase in the level of IAA oxidase activity at high level of tissue Mn was accompanied by simultaneous decrease in the concentration of o-dihydroxyphenols. These results indicate the possible involvement of phenols in the inhibition of IAA oxidase in the leaves of strawberry plants and manganese seems to affect the levels of the inhibitor(s).