Metabolic involvement in acid-mediated extension growth of maize coleoptiles

Abstract

The acid-growth response (AGR) induced by acidic buffer (pH 4) in abraded maize (Zea mays L.) coleoptile segments can be completely inhibited within a few minutes by inhibitors of the haemoprotein function (KCN, Na-azide) or ionophores collapsing the proton gradients across membranes (carbonyl cyanide m-chlorophenyl hydrazone, monensin). These substances also interfere with the acid-mediated increase in cell-wall extensibility measured with a constant-load extensiometer in vivo in turgid or non-turgid segments, but have no effect on the extensibility of the cell walls measured in vitro with frozen/thawed segments. The inhibitors do not cause an alkalinization of the apoplastic solution or a decrease in the osmotic pressure of the cell sap of acid-treated segments. In contrast, inhibitors of ATP synthesis (N,N'-dicyclohexyl-carbodiimide, diethylstilbestrol), which arrest auxin-mediated growth in a similar way to KCN, have no effect on AGR. Removal of O 2 inhibits growth at pH 4 by about 25%; the anoxia-insensitive part of the AGR can be fully inhibited by azide. Diminishing the membrane potential with valinomycin has no effect on AGR. It is concluded that the AGR is controlled by protoplastic functions, possibly localized in the plasma membrane, which are lost when the cells are killed. The isolated cell wall may not represent a sufficient model system for the biochemical mechanism of AGR.