Hypocotyls of Cucurbita pepo L. (zucchini) seedlings grown at low calcium levels (0.1 mM) showed reduced basipetal polar transport of the auxins indole-3-acetic acid and 1-naphthylacetic acid in comparison with control plants grown at 5 mM Ca(2+). The contribution to overall transmembrane auxin transport of the symport uptake carrier was unchanged by calcium deficiency, but the efflux carrier of the auxin-anion uniport was less active and the sensitivity of auxin transport to N-1-naphthylphthalamic acid (NPA) inhibition was thereby reduced. These changes could partially be reversed by short treatments with Ca(2+) or La(3+). The NPA receptor was unaltered in level and affinity for NPA by calcium deficiency. It is suggested that the major lesion responsible for diminished polar auxin transport in calcium-deficient tissue is in flux through the auxin efflux carrier which could be subject to control by Ca(2+) by as yet unestablished mechanisms.