Abstract
The plant hormone auxin (Indole-3-Acetic Acid, IAA) is a key player in nearly every aspect of plant growth and development ranging from cell division and cell elongation to embryogenesis and root formation. The IAA level in specific tissues and cells is regulated by synthesis, conjugation, degradation and transport. Especially long-range polar auxin transport (PAT) has been the subject of numerous studies. The chemi-osmotic theory predicts that intercellular PAT is caused by an asymmetric distribution of auxin efflux transporters in cell membranes of transporting cells, resulting in increased local membrane permeability for IAA. Members of the PIN gene family are generally considered to encode the postulated carriers. The objective of this study was to use the chemi-osmotic theory in an experimental program aimed at describing and interpreting long-range PAT data from mutants of the PIN gene family of Arabidopsis thaliana. Therefore, we put the chemi-osmotic theory in a broader theoretical framework. We find that the observed decrease in both auxin flux and transport velocity in pin1 loss-of-function mutants is not caused by decreased basal membrane permeability, as would be expected according to the chemi-osmotic theory, but is an indirect effect caused by a change in the dynamics of auxin transport due to a decrease in the expression of all four AUX1/LAX1-3 auxin influx carriers in pin1 mutants. On the basis of our findings, we conclude that the exact role of PIN1 in long-distance PAT, as postulated in the chemi-osmotic theory, should be reconsidered.