The uptake of [1-14C]IAA (0-20 .mu.M) into light-grown pea stem segments was measured under various conditions to determine which mechanisms of auxin transport in crown gall suspension culture cells were also found in a tissue capable of polar auxin transport. IAA uptake increased as the external pH was lowered; it was less than that of benzoic acid (BA), naphthylacetic acid (NAA) or under equivalent conditions. TIBA [2,3,5-triiodobenzoic acid] enhanced net IAA uptake through inhibition of efflux, and to a lesser extent, also increased uptake of NAA and 2,4D while it had no effect on BA uptake. Both DNP [2,4-dinitrophenol] and, at higher concentrations, BA, reduced IAA uptake because of a cytoplasmic pH reduction. However, low concentrations of both BA and DNP caused a slight enhancement of IAA net uptake, possibly through a reduction of carrier-mediated IAA efflux. With TIBA, the inhibitory effects of DNP and BA were more severe and no enhancement of uptake was at low concentrations. Non-radioactive IAA (10 .mu.M) reduced uptake of labeled IAA. It further increased in concentration to 1.0 mM, but first produced an inhibition (0-10 min) of labeled IAA uptake, then a stimulation later. Non-radioactive 2,4 D decreased, but did not stimulate uptake of labeled IAA. With TIBA, labeled IAA uptake was inhibited by non-radioactive IAA regardless of its concentration. Sulphydryl reagents PCMB [p-chloromercuribenzoic acid] and PCMBS [p-chloromercuribenzene sulfonic acid] promoted or inhibited IAA uptake depending, respectively, on penetration or exclusion from the cells. The penetrant PCMB reduced the promotion of labeled IAA uptake by TIBA or high concentrations of added non-labeled IAA. The findings were consistent with the diffusive entry of unionised IAA into cells together with some carrier-mediated uptake. Auxin efflux from the cells appears to have a carrier-mediated contribution, partly inhibited by TIBA, which has a capacity at least as great as the uptake carrier. Apparently, pea stem segments contain cells whose mechanisms of trans-membrane auxin transport fit the model of polar auxin transport proposed from experiments with crown gall suspension cells, although differences, particularly of carrier specificity, are apparent between the 2 systems.