Abstract

The development of lateral roots in Arabidopsis thaliana is strongly dependent on signaling directed by the AUXIN RESPONSE FACTOR7 (ARF7), which in turn activates LATERAL ORGAN BOUNDARIES DOMAIN (LBD) transcription factors (LBD16, LBD18 and LBD29). Here, the product of PRH1, a PR-1 homolog annotated previously as encoding a pathogen-responsive protein, was identified as a target of ARF7-mediated auxin signaling and also as participating in the development of lateral roots. PRH1 was shown to be strongly induced by auxin treatment, and plants lacking a functional copy of PRH1 formed fewer lateral roots. The transcription of PRH1 was controlled by the binding of both ARF7 and LBDs to its promoter region.

Highlights

  • The architecture of the root system depends on the density of lateral roots (LRs) formed along with the extent of root branching

  • To identify additional targets involved in AUXIN RESPONSE FACTOR7 (ARF7)-mediated auxin signaling and LR development (Fig 1A and 1B), a comparison was made between the 8-day-old wild type (WT) or arf7 mutant seedlings exposed to 10 μM naphthalene acetic acid (NAA) for 4 hours respectively (Figs 1C and S1A)

  • The differentially expressed genes (DEGs) were selected based on the comparisons (WT-NAA VS WT-Mock, arf7-NAA VS arf7-Mock, arf7-Mock VS WT-Mock, arf7-NAA VS WT-NAA), which were induced by auxin and regulated by ARF7

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Summary

Introduction

The architecture of the root system depends on the density of lateral roots (LRs) formed along with the extent of root branching. LRs are initiated from mature pericycle cells lying adjacent to the xylem pole, referred to in Arabidopsis thaliana as the xylem pole pericycle [1, 2]. A subset of these cells, namely the founder cells, undergo a series of highly organized divisions to form an LR primordium, which eventually develops into an LR. Functional analysis of AtPRH1 in A. thaliana. Fundamental Research Funds of Shandong University (No 2016GN021). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

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