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. Five-cm apical segments 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 is therefore not through a secreted antiauxin. The second hypothesis was that the fungus metabolizes or otherwise reduces the effectiveness of auxin. This was tested by measuring growth of both 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%. There was again 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.