Abstract

Although research has determined that reactive oxygen species (ROS) function as signaling molecules in plant development, the molecular mechanism by which ROS regulate plant growth is not well known. An aba overly sensitive mutant, abo8-1, which is defective in a pentatricopeptide repeat (PPR) protein responsible for the splicing of NAD4 intron 3 in mitochondrial complex I, accumulates more ROS in root tips than the wild type, and the ROS accumulation is further enhanced by ABA treatment. The ABO8 mutation reduces root meristem activity, which can be enhanced by ABA treatment and reversibly recovered by addition of certain concentrations of the reducing agent GSH. As indicated by low ProDR5:GUS expression, auxin accumulation/signaling was reduced in abo8-1. We also found that ABA inhibits the expression of PLETHORA1 (PLT1) and PLT2, and that root growth is more sensitive to ABA in the plt1 and plt2 mutants than in the wild type. The expression of PLT1 and PLT2 is significantly reduced in the abo8-1 mutant. Overexpression of PLT2 in an inducible system can largely rescue root apical meristem (RAM)-defective phenotype of abo8-1 with and without ABA treatment. These results suggest that ABA-promoted ROS in the mitochondria of root tips are important retrograde signals that regulate root meristem activity by controlling auxin accumulation/signaling and PLT expression in Arabidopsis.

Highlights

  • Plant growth and development are greatly influenced by the accumulation of reactive oxygen species (ROS), which are produced under environmental stresses such as water deficiency and high salinity [1,2,3,4]

  • abscisic acid (ABA)-inhibition of root growth and germination was greater in abo8-1 and abo8-2 than in the wild type (Fig. 1A–E)

  • These results demonstrate that mutations in ABO8 retard plant growth and causes ABA hypersensitivity in Arabidopsis

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Summary

Introduction

Plant growth and development are greatly influenced by the accumulation of reactive oxygen species (ROS), which are produced under environmental stresses such as water deficiency and high salinity [1,2,3,4]. The triple mutant with disruption of two NADPlinked thioredoxin reductase gene (NTRA and NTRB) and CAD2/RML1 results in altered auxin homeostasis and reduced root growth [16]. The auxin-receptor mutants tir afb and tir afb are more resistant to oxidative stress and produce less ROS under salt treatment than the wild type [17]. The accumulation of ROS in the mutant of ABO6 (ABA Overly sensitive 6 encodes a DEXH box RNA helicase that regulates the splicing of genes in complex I) disrupts auxin homeostasis and inhibits root growth under ABA treatment [19]. The oxidation of active indole-3-acetic acid (IAA) into the low activity 2-oxindole-3-acetic acid (OxIAA) mainly occurs in the root apex in Arabidopsis and should play crucial roles in auxin homeostasis for regulating root growth [20]

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