, Volume 118, Issue 2, pp 101-121

Carrier-mediated auxin transport

Summary

  1. Auxin (IAA) transport was investigated using crown gall suspension tissue culture cells. We have shown that auxin can cross the plasmalemma both by transport of IAA anions on a saturable carrier and by passive (not carriermediated) diffusion of the lipid-soluble undissociated IAA molecules (pK=4.7). The pH optimum of the carrier for auxin influx is about pH 6 and it is half-saturated by auxin concentrations in the region of 1–5 μM. We found that the synthetic auxin 2,4D specifically inhibited carrier-mediated IAA anion influx, and possibly also efflux. Other lipid-soluble weak acids which are not auxins, such as 3,4-dichlorobenzoic acid, had no effect on auxin transport. By contrast, we found that TIBA, an inhibitor of polar auxin transport in intact tissues inhibited only the carrier-mediated efflux of IAA.

  2. When the pH outside the cells is maintained below that of the cytoplasm (pH 7), auxin can be accumulated by the cells: In the initial phase of uptake, the direction of the auxin concentration gradient allows both passive carrier-mediated anion influx (inhibited by 2,4D) and a passive diffusion of undissociated acid molecules into the cells. Once inside the cytoplasm, the undissociated molecules ionise, producing IAA anions, to a greater extent than in the more acidic extracellular environment. Uptake by passive diffusion continues as long as the extracellular concentration of undissociated acid remains higher than its intra-cellular concentration. Thus, the direction of the auxin anion concentration gradient is reversed after a short period of uptake and auxin accumulates within the cells. The carrier is now able to mediate passive IAA anion efflux (inhibited by TIBA) down this concentration gradient even though net uptake still proceeds because the carrier is saturable whereas passive diffusion is not.

  3. Auxin “secretion” from cells is regarded as a critical step in polar auxin transport. The evidence which we present is consistent with the view that auxin “secretion” depends on a passive carrier-mediated efflux of auxin anions which accumulate within the cells when the extra-cellular pH is below that of the cytoplasm. The implications of this view for theories of polar auxin transport are discussed.

This work was carried out during the tenure by A. R. Sheldrake of the Royal Society Rosenheim Research Fellowship.