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Original Articles

Iron‐deficiency stress responses of a chlorosis‐susceptible and a chlorosis‐resistant cultivar of muskmelon as related to root riboflavin excretion

Pages 1157-1169 | Published online: 21 Nov 2008
 

Abstract

Cultivar Edisto and an Fe‐inefficient mutant (fefe) muskmelon were noted by Jolley et al. (1991) to differ with Fe‐deficiency stress in their ability to lower their nutrient solution pH, to increase their root Fe‐reductive capacity, to transport Fe to leaves, and to develop chlorosis. These two muskmelon cultivars were Fe‐stressed along with controls, and daily measurements for nutrient solution pH and riboflavin concentrations were taken. Root Fe‐reductive activity and apical leaf chlorophyll content was measured on selected days. Riboflavin excretion by Fe‐deficiency stressed Edisto plants increased by the second day, reached a peak after seven days and declined slightly. Edisto plants with Fe excreted 100 to 300 times less riboflavin than those without Fe. The fefe Fe‐deficiency stressed plants and those with Fe excreted similar very low amounts of riboflavin several fold less than the Edisto plants with Fe. The nutrient solution pH was decreased by Fe‐stressed Edisto plants from pH 5.0 to 3.7, whereas the nutrient solution pH of Edisto plants with Fe increased to pH 7 or less. The nutrient solution of fefe plants with and without Fe increased to pH 7.7 and remained high or decreased. The decrease in chlorophyll of apical leaves of fefe plants without Fe were more rapid and more pronounced than those of Edisto. Pronounced increases in root Fe‐reduction capacity developed only with the Fe‐stressed Edisto plants and was associated in time with the pH decrease and major riboflavin excretion. The efficiency of photo‐reduced riboflavin to reduce FeIII‐EDTA was related to the amount of riboflavin excreted in one h or over days and to the amount of root‐Fe‐reductive capacity in one h. The possibility of epidermal cell riboflavin participating as an intermediate in a plasmalemma NAD(P)H ‐ Fe chelate reductase is discussed.

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