Abstract

Amaranthus palmeri S. Watson (Palmer amaranth) is considered a problematic and troublesome weed species in many crops in the USA, partly because of its ability to evolve resistance to herbicides. In this study, we explored the mechanism of resistance in a trifluralin-resistant A. palmeri accession collected from Arkansas, USA. Dose-response assays using agar plates demonstrated an EC50 (effective concentration that reduces root length by 50%) of 1.02 µM trifluralin compared to 0.39 µM obtained in the susceptible accession. Thus, under these conditions, the resistant accession required 2.6 times more trifluralin to inhibit root length by 50%. Seeds in the presence or absence of the cytochrome P450-inhibitior malathion displayed a differential response with no significant influence on root length, suggesting that resistance is not P450-mediated. In addition, application of 4-chloro-7-nitrobenzofurazan (NBD-Cl), a glutathione S-transferase (GST) inhibitor, showed significant differences in root length, indicating that GSTs are most likely involved in the resistance mechanism. Sequencing of α- and β-tubulin genes revealed no single nucleotide polymorphisms (SNPs) previously described between accessions. In addition, relative gene copy number of α- and β-tubulin genes were estimated; however, both resistant and susceptible accessions displayed similar gene copy numbers. Overall, our results revealed that GST-mediated metabolism contributes to trifluralin resistance in this A. palmeri accession from Arkansas.

Highlights

  • A. palmeri, a dicotyledonous species native to southwestern USA, is one of the most troublesome weeds of agronomic crops in the USA [1,2]

  • Different herbicides have been used for its control, and overreliance has gradually led to the appearance of A. palmeriresistant accessions [3]

  • Dose-Response Experiments on Agar Plates. Root length in both accessions decreased as the trifluralin concentration increased, and at 10 DAT visual differences were clearly observed between accessions

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Summary

Introduction

A. palmeri, a dicotyledonous species native to southwestern USA, is one of the most troublesome weeds of agronomic crops in the USA [1,2]. Different herbicides have been used for its control, and overreliance has gradually led to the appearance of A. palmeriresistant accessions [3]. A. palmeri accessions with multiple resistance to herbicides have frequently been reported. Trifluralin (α, α, α -trifluoro-2,6-dinitro-N,N-dipropyl-p-toluidine), was first commercially released in 1964 to control grass and dicotyledonous weeds using preplant soil incorporated applications in different row cropping systems [12]. Trifluralin is a member of the dinitroaniline herbicide family, inhibiting microtubule (formed by the α- and β-tubulin heterodimers) assembly/polymerization. Inhibition of microtubule assembly/polymerization causes a mitosis alteration that triggers growth interruption and plant death [15,16]. Suppression in the synthesis of DNA, RNA and protein have been reported in the presence of trifluralin [18]

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