Abstract
Most dicotyledonous species respond to Fe deficiency by developing several mechanisms known as Fe-deficiency stress responses. To study the regulation of these responses, young cucumber plants (Cucumis sativus L. cv Ashley) were grown in nutrient solution for 11 d, being deprived of Fe during the last 4 or 5 d. Inhibitors of ethylene synthesis (2 or 10 [mu]M aminoethoxyvinylglycine; 10 or 20 [mu]M aminooxyacetic acid; 1, 2, 5, or 10 [mu]M Co2+ as CoCl2) or action (50, 200, or 800 [mu]M Ag+ as silver thiosulfate) were added to the nutrient solution at different times during this period of growth with no Fe. After this period, the reduction of Fe3+ ethylenedi-aminetetraacetate by the roots of entire plants was measured with ferrozine by reading the absorbance at 562 nm after 2 h. The presence of the ethylene inhibitors in the nutrient solution inhibited the Fe-deficiency stress responses ferric-reducing capacity and subapical root swelling. In another experiment, the addition of 1 [mu]M 1-aminocyclopropane-1-carboxylic acid (ACC), a precursor of ethylene synthesis, to the nutrient solution of plants having low ferric-reducing activity increased notably the ferric-reducing capacity and subapical root swelling. Here we show evidence that ethylene plays a role in the development of Fe-deficiency stress responses, since when ethylene synthesis or action was inhibited, the responses were also inhibited, and when a precursor of ethylene (ACC) was added, the responses were increased.