Cyanide Inhibition of Acid-induced Growth in Avena Coleoptile Segments

Abstract

The comparative effects of metabolic inhibitors on acid-and auxininduced growth in oat (Avena sativa L. var. Victory) coleoptile segments have been examined. Acid (pH 4)-induced growth in both peeled and unpeeled segments is inhibited by 1 millimolar KCN when added at the time of acidification. KCN inhibits total acid-induced growth by 59 and 76%, respectively, in peeled and nonpeeled segments during the first 60 minutes. The growth rate of cyanide-treated tissue drops to zero or near zero in both peeled and nonpeeled segments during this period. Cyanide inhibition of total acid-induced growth in peeled segments at pH 5 is even more severe, amounting to about 80% during the first 60 mniutes. The possibility that inhibition by cyanide may be caused by some nonspecific effect of the inhibitor on a process other than respiration, e.g. turgor reduction due to membrane damage, has not been rled out. Acidinduced growth is also inhibited by 3 millimolar sodium fluoride and by anoxia. In unpeeled segments total pH 4-induced growth is inhibited 73% by sodium fluoride and 38% by anoxia during the 1st hour. Possible corrections to the above inhibition percentages which may be necessary due to the sensitivity of basal growth to inhibitors are discussed. Cyanide was found to inhibit auxin-induced growth much more rapidly than acid-induced growth. These data suggest that acid growth may be dependent on respiratory metabolism but to a lesser degree than is auxin-induced growth. If the acid growth theory of auxin action is correct, it appears that there may be two steps in the growth process which are dependent on respiratory metabolism: (a) auxin-induced proton pumping which is highly sensitive to respiratory inhibitors; and (b) acid-mediated wail loosening which is moderately and perhaps indirectly sensitive to respiratory inhibitors.The rapid elongation of stem and coleoptile segments in response to auxin has been described as an active process which is very sensitive to metabolic inhibitors (14, 15). According to the acid growth hypothesis, auxin is thought to activate a metabolically driven proton pump which excretes H+ into the cell wall (5, 18). The resultant decrease in wall pH is thought to cause wall loosening which is followed by turgor-driven growth. The rapid suppressive effect (e.g. 2-10 min, see refs. 13 and 15) of respiratory inhibitors on auxin-induced growth may be caused by their ability to interfere with oxidative phosphorylation, thus deactivating the proton pump. The resulting increase in cell wall pH may be responsible for the observed cessation of wall loosening and growth.-In contrast, the rapid elongation of stem and coleoptile segments in response to external application of acid has been described as a passive process which is dependent upon turgor but insensitive to metabolic inhibitors and anaerobic conditions (14). More recently, it has been described as an enzymic wall-loosening process which is insensitive to metabolic inhibitors (18). The enhancement of growth by acid has been considered...