THE CURRENT STATUS OF THE ACID-GROWTH HYPOTHESIS

Excised coleoptile segments that were depleted of endogenous auxin aft er pre-incubation in water respond to the phytotoxin fusicoccin (FC) a nd the plant hormone auxin (indole-3-acetic acid, IAA) with an enhance ment of growth. This promotion of organ elongation is caused by an inc rease in the extensibility of the thick, growth-limiting outer epiderm al wall. The acid-growth hypothesis postulates that both FC and IAA ca use wall-loosening and the concomitant induction of growth by rapid ac idification of the extension-limiting cell wall. At saturating concent rations FC and IAA cause very similar growth responses. However, the e quilibrium-pH in the incubation medium (similar to pH Of the periphera l 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-media ted 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 with the water-control. FC-mediated growth can be inh ibited by neutral buffers infiltrated into the outer epidermal wall, b ut a substantial growth response occurs after addition of IAA under id entical conditions. A suboptimal concentration of FC was used to mimic the effect of IAA on acid secretion. When a pH of 4.8-5.0 was establi shed by FC in the peripheral wall no promotion of growth occurred. Hen ce, IAA-induced proton excretion is insufficient to cause cell-wall lo osening in the coleoptile. Abraded segments that rapidly elongate in a cid buffers (pH 3.5-4.0) respond to IAA with an additional enhancement of growth, but under identical conditions FC is without effect. The g rowth-promoting effects of acid and IAA are additive, i.e. IAA and aci d act via separate mechanisms. These results are consistent with the a cid-growth hypothesis of FC action. However, they indicate that IAA in duces growth by a mechanism independent of cell-wall acidification. Al ternative hypotheses of IAA-mediated cell-wall loosening are discussed .