1. Zentrum für Molekularbiologie der Pflanzen, Universität Tübingen, Auf der Morgenstelle 3, D-72076 Tübingen, Germany
2. Max-Delbrück-Laboratorium in der Max-Planck-Gesellschaft, D-50829 Köln, Germany
3. Department of Biochemistry, Faculty of Science, Masaryk University, Kotlárská 2, 61137 Brno, Czech Republic
4. These authors contributed equally to this work
5. Present address: Zentrum für Molekularbiologie der Pflanzen, Universität Tübingen, Auf der Morgenstelle 3, D-72076 Tübingen, Germany.

Correspondence to: Gerd Jürgens¹ Correspondence and requests for materials should be addressed to G.J. (e-mail: Email: gerd.juergens@zmbp.uni-tuebingen.de).

Abstract

Polar transport of the phytohormone auxin mediates various processes in plant growth and development, such as apical dominance, tropisms, vascular patterning and axis formation^{1, 2}. This view is based largely on the effects of polar auxin transport inhibitors. These compounds disrupt auxin efflux from the cell but their mode of action is unknown³. It is thought that polar auxin flux is caused by the asymmetric distribution of efflux carriers acting at the plasma membrane⁴. The polar localization of efflux carrier candidate PIN1 supports this model⁴. Here we show that the seemingly static localization of PIN1 results from rapid actin-dependent cycling between the plasma membrane and endosomal compartments. Auxin transport inhibitors block PIN1 cycling and inhibit trafficking of membrane proteins that are unrelated to auxin transport. Our data suggest that PIN1 cycling is of central importance for auxin transport and that auxin transport inhibitors affect efflux by generally interfering with membrane-trafficking processes. In support of our conclusion, the vesicle-trafficking inhibitor brefeldin A mimics physiological effects of auxin transport inhibitors.