[Changes in soluble sugar and cell-wall carbohydrate content during inhibition of endogenous cell elongation by antimetabolites].

The effect of actinomycin D, hydroxyproline, cycloheximide, and chloramphenicol on the soluble sugar and cell-wall carbohydrate content was studied in an effort to look for the primary action of these antimetabolites on the cell-wall in connection with cell elongation during inhibition of endogenous hypocotyl growth in mustard seedlings (Sinapis alba L.). The experiments have been done under steady state conditions as far as the parameters under examination are concerned. During the experimental period hypocotyl elongation is due almost exclusively to cell elongation (GEISER, 1964). Antimetabolite concentrations in an 1 hr feeding period have been chosen to effect about 70% relative inhibition 12 hrs after feeding.All antimetabolites confermably caused hypocotyl inhibition already about 1 hr after the beginning of their application. Cycloheximide and chloramphenicol inhibited or impaired fructose and glucose accumulation 1-2 hrs, and cell-wall carbohydrate synthesis about 3 hrs after the onset of hypocotyl inhibition. In contrast, actinomycin D and hydroxyproline leave fructose and glucose accumulation unchanged up to 9 hrs, but they do inhibit cell-wall carbohydrate synthesis approximately as fast as they inhibit hypocotyl elongation. However, the relative inhibition of cell-wall carbohydrate synthesis is only 1/3 of the relative inhibition of hypocotyl elongation.A comparison of the lag-phases and the courses of the kinetics reveals that the changes in the soluble sugar and cell-wall carbohydrate content starting 3-4 hrs after antimetabolite application are only secondary changes not directly concerned with the primary processes leading to hypocotyl inhibition. From the far reaching independence of hypocotyl inhibition and cell-wall carbohydrate synthesis during the first hours after feeding, the conclusion can be drawn that in the case of cycloheximide and chloramphenicol the primary inhibition of hypocotyl elongation must be due to changes in the structural arrangement of cell-wall elements and not to any kind of inhibition of the synthesis of cell-wall carbohydrates. In the case of actinomycin D and hydroxyproline also at least the greatest part of the inhibition, if not all of it, must also be mediated by the same process. Though secondary changes observed in soluble sugar and cell-wall carbohydrate content point to rather different patterns of antimetabolite action, the primary action on the cell-wall in connection with cell growth inhibition, according to the present data, seems to be generally the same regardless of which inhibitor is used.