Proton efflux from oat coleoptile cells and exchange with wall calcium after IAA or fusicoccin treatment.

Elongation growth of plant cells occurs by stretching of cell walls under turgor pressure when intermolecular bonds in the walls are temporarily loosened. The acid-growth theory predicts that wall loosening is the result of wall acidification because treatments (including IAA and fusicoccin) that cause lowered wall pH cause elongation. However, conclusive evidence that IAA primarily reduces wall pH has been lacking. Calcium has been reported to stiffen the cell walls. We have used a microelectrode ion-flux measuring technique to observe directly, and non-invasively, the net fluxes of protons and calcium from split coleoptiles of oats (Avena sativa L.) in unbuffered solution. Normal net fluxes are 10 nmol · m(-2) · s(-1) proton efflux and zero calcium flux. The toxin fusicoccin (1 μM) causes immediate efflux from tissue not only of protons, but also of calcium, about 110 nmol · m(-2) · s(-1) in each case. The data fit the "weak acid Donnan Manning" model for ion exchange in the cell wall. Thus we associate the known "acid-growth" effect of fusicoccin with the displacement of calcium from the wall by exchange for protons extruded from the cytoplasm. Application of 10 μM IAA causes proton efflux to increase transiently by about 15 nmol · m(-2) · s(-1) with a lag of about 10 min. The calcium influx decreases immediately to an efflux of about 20 nmol · m(-2) · s(-1). It appears that auxin too causes an "acid-growth" effect, with extruded protons exchanging for calcium in the cell walls.