The dynamics of H+ efflux from the trap lobes of Dionaea muscipula Ellis (Venus's flytrap)

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Abstract
H+ efflux from the trap lobes of Dionaea muscipula Ellis (Venus's flytrap) was measured in vitro. FC, IAA, and 2,4‐D markedly increase the rate of H+ efflux within minutes of their addition to the incubation medium whereas ABA and DES cause the rate to decrease. Consequently, the H+ efflux mechanism of Dionaea is considered to be similar to the H+ extrusion pumps of other higher plants in this respect. However, the H+ extrusion mechanism of Dionaea may be unusual in that long‐term exposure of the trap lobes to known secretion elicitors— bactopeptone, NH4+, Na +, urea, thiourea, glycine or xanthine—also causes a large increase in the steady‐state rate of H+ efflux from the trap lobes. Since the observed H+ effluxes primarily correspond to the adaxial surface of the trap lobes and show similar time‐ and secretion elicitor‐dependencies to the responses seen in situ, it appears that the H+ effluxes measured in vitro bear a direct relationship to those observed in the intact, actively secreting plant.Three of the secretion elicitors that were tested— K+, NH4+, and urea—have rapid effects on the rate of H+ extrusion in addition to their long‐term effects. K+ and NH4+ cause a rapid acceleration of H+ efflux whereas urea causes a rapid deceleration or, at high external concentrations, reversal of the net flux. The effect of K+ is inferred to result from K+ ‐H+ exchange between the tissue and bathing medium. Studies with structural analogues of NH4+ and urea and inhibitors of the assimilation of reduced nitrogen suggest that the effects of NH4+ and urea result from the pH‐perturbing consequences of their metabolism subsequent to their absorption. These effects are considered to be auxiliary to the elicitation of secretion.It is proposed that H+ efflux from the trap lobes is mediated by a K+‐H+ exchange mechanism, the activity of which is modified by long‐term exposure to secretion elicitors and/or short‐term exposure to factors which alter the availability of endogenous H+ ions.