Cellular auxin levels are determined by processes including synthesis, degradation, and conjugation, as well as by auxin transport across the plasma membrane. Whereas transport of free auxins such as naturally occurring IAA is well characterized, little is known about the transport of auxin precursors and metabolites. Here, we identify amutation in the ABCG37 gene of Arabidopsis that causes the polar auxin transport inhibitor sensitive1 (pis1) phenotype manifested by hypersensitivity to auxinic compounds. ABCG37 encodes the pleiotropic drug resistance transporter that transports a range of synthetic auxinic compounds as well as the endogenous auxin precursor indole-3-butyric acid (IBA), but not free IAA. ABCG37 and its homolog ABCG36 act redundantly at outermost root plasma membranes and, unlike established IAA transporters from the PIN and ABCB families, transport IBA out of the cells. Our findings explore possible novel modes of regulating auxin homeostasis and plant development.