Auxin-Induced Plasma Membrane Depolarization Is Regulated by Auxin Transport and Not by AUXIN BINDING PROTEIN1.

Ivan A Paponov,Rainer Hedrich,Vadym Budnyk,Elżbieta Król,Martina Paponov,William Teale,Tatyana Friz,Klaus Palme,Julian Dindas

doi:10.3389/fpls.2018.01953

Abstract

Auxin is a molecule, which controls many aspects of plant development through both transcriptional and non-transcriptional signaling responses. AUXIN BINDING PROTEIN1 (ABP1) is a putative receptor for rapid non-transcriptional auxin-induced changes in plasma membrane depolarization and endocytosis rates. However, the mechanism of ABP1-mediated signaling is poorly understood. Here we show that membrane depolarization and endocytosis inhibition are ABP1-independent responses and that auxin-induced plasma membrane depolarization is instead dependent on the auxin influx carrier AUX1. AUX1 was itself not involved in the regulation of endocytosis. Auxin-dependent depolarization of the plasma membrane was also modulated by the auxin efflux carrier PIN2. These data establish a new connection between auxin transport and non-transcriptional auxin signaling.

Highlights

In plants, indole-3-acetic acid (IAA), the most abundant naturally occurring auxin, plays a central role in orchestrating a wide range of context-dependent growth and developmental processes (Teale et al, 2006)
AUXIN BINDING PROTEIN1 (ABP1) Is Not Involved in Auxin-Induced Plasma Membrane Depolarization
The lack of visible phenotypes in qualified null abp1 alleles led us to revisit the question of whether depolarization of the plasma membrane and endocytosis are initiated by the binding of auxin to ABP1

Summary

Introduction

Indole-3-acetic acid (IAA), the most abundant naturally occurring auxin, plays a central role in orchestrating a wide range of context-dependent growth and developmental processes (Teale et al, 2006). Transgenic approaches, which increased or reduced expression of ABP1 using conditional ectopic expression or antisense approaches, did not reveal any ABP1-dependent phenotypes (Feckler, Palme, unpublished data). When it was reported in 2001 that a T-deoxyribonucleic acid insertion in ABP1 caused embryo lethality (Chen et al, 2001), it seemed clear that ABP1 was the sole receptor for at least one crucial auxin-related process. This led to efforts in which weak alleles of abp were isolated or

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