Auxin transport inhibitors block PIN1 cycling and vesicle trafficking

Niko Geldner, Jiří Friml, York-Dieter Stierhof, Gerd Jürgens () and Klaus Palme
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Niko Geldner: Zentrum für Molekularbiologie der Pflanzen, Universität Tübingen
Jiří Friml: Max-Delbrück-Laboratorium in der Max-Planck-Gesellschaft
York-Dieter Stierhof: Zentrum für Molekularbiologie der Pflanzen, Universität Tübingen
Gerd Jürgens: Zentrum für Molekularbiologie der Pflanzen, Universität Tübingen
Klaus Palme: Max-Delbrück-Laboratorium in der Max-Planck-Gesellschaft

Nature, 2001, vol. 413, issue 6854, 425-428

Abstract: Abstract Polar transport of the phytohormone auxin mediates various processes in plant growth and development, such as apical dominance, tropisms, vascular patterning and axis formation1,2. 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.

Date: 2001
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DOI: 10.1038/35096571

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