The current status of the acid‐growth hypothesis

Abstract

SUMMARYExcised coleoptile segments that were depleted of endogenous auxin after pre‐incubation in water respond to the phytotoxin fusicoccin (FC) and the plant hormone auxin (indole‐3‐acetic acid, IAA) with an enhancement of growth. This promotion of organ elongation is caused by an increase in the extensibility of the thick, growth‐limiting outer epidermal wall. The acid‐growth hypothesis postulates that both FC and IAA cause wall‐loosening and the concomitant induction of growth by rapid acidification of the extension‐limiting cell wall. At saturating concentrations FC and IAA cause very similar growth responses. However, the equilibrium‐pH in the incubation medium (∼ pH of the peripheral cell wall) of abraded FC‐treated segments is 3.5–4.0, whereas in the presence of IAA a pH of 4.8–5.0 is established. The FC‐ and IAA‐mediated induction of growth can be stimulated by an external buffer of pH 3.5–4.0. Acid buffers of pH 5, however, cause almost no enhancement of growth compared WJth the water‐control. FC‐mediated growth can be inhibited by neutral buffers infiltrated into the outer epidermal wall, but a substantial growth response occurs after addition of IAA under identical conditions. A sub‐optimal concentration of FC was used to mimic the effect of IAA on acid secretion. When a pH of 4.8–5.0 was established by FC in the peripheral wall no promotion of growth occurred. Hence, IAA‐induced proton excretion is insufficient to cause cell‐wall loosening in the coleoptile. Abraded segments that rapidly elongate in acid buffers (pH 3.5–4.0) respond to IAA with an additional enhancement of growth, but under identical conditions FC is without effect. The growth‐promoting effects of acid and IAA are additive, i.e. IAA and acid act via separate mechanisms. These results are consistent with the acid‐growth hypothesis of FC action. However, they indicate that IAA induces growth by a mechanism independent of cell‐wall acidification. Alternative hypotheses of IAA‐mediated cell‐wall loosening are discussed. Contents Summary 549 I. Introduction 550 II. Segment elongation and the organismal concept of multicellularity 550 III. FC‐ and IAA‐mediated acid secretion 552 IV. The acid‐growth hypothesis of FC action 555 V. The acid‐growth hypothesis of IAA action 560 VI. Conclusions 567 Acknowledgements 568