Sweet corn roots colonized with the T-22 strain of the common rhizosphere fungus grow substantially faster than roots of plants not so colonized. We tested whether this growth enhancement was a consequence of the fungus affecting auxin regulation of cell elongation. In corn roots, auxin acts an inhibitor of growth, maintaining the rate below its short-term maximum potential. The first hypothesis was that the fungus secretes an auxin inhibitor, and thereby reduces the auxin limitation of growth. Apical segments (5 cm) were incubated in media conducive to elongation, supplemented with 0.1 μm indole acetic acid (IAA), a T-22 culture filtrate (5%), or both. IAA inhibited growth by 69%, and the culture filtrate inhibited by 16% with no interaction. The action of T-22, therefore, is not through a secreted antiauxin. The second hypothesis was that the fungus metabolizes or otherwise reduces the effectiveness of auxin, which was tested by measuring growth of colonized and uncolonized seedlings after a half-hour incubation of the root tips in 0.1 μm IAA. Auxin inhibited growth by 42%, whereas colonization increased growth by 27%. Again, there was no interaction, a result inconsistent with the antiauxin model. The third experiment further tested the antiauxin hypothesis by maximizing acid growth (normally regulated by auxin) by incubating the root tips in 1 μm fusicoccin (FC). Colonization increased growth by 10% without FC but by 42% with it. FC alone increased growth by 11%. The significant positive interaction is not consistent with a change in the auxin sensitivity but is consistent with an increase in the maximum sustainable growth rate.