PPO2 Mutations in Amaranthus palmeri: Implications on Cross-Resistance

Pâmela Carvalho-Moore,Douglas Findley,Nilda Roma-Burgos,James Heiser,Gulab Rangani,Steven J Bowe

doi:10.3390/agriculture11080760

Pâmela Carvalho-Moore, Douglas Findley + Show 4 more

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https://doi.org/10.3390/agriculture11080760

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Abstract

In Arkansas, resistance to protoporphyrinogen IX oxidase (PPO)-inhibiting herbicides in Amaranthus palmeri S. Wats. is mainly due to target site mutations. Although A. palmeri PPO-mutations are well investigated, the cross-resistance that each ppo mutant endows to weed populations is not yet well understood. We aimed to evaluate the response of PPO-resistant A. palmeri accessions, harboring the ppo2 mutations ΔG210 and G399A, to multiple PPO-inhibiting herbicides. Six resistant and one susceptible field accessions were subjected to a dose–response assay with fomesafen, and selected survivors from different fomesafen doses were genotyped to characterize the mutation profile. The level of resistance to fomesafen was determined and a cross-resistance assay was conducted with 1 and 2 times the labeled doses of selected PPO herbicides. The accession with higher predicted dose to control 50% of the population (ED50) had a higher frequency of ΔG210-homozygous survivors. Survivors harboring both mutations, and those that were ΔG210-homozygous, incurred less injury at the highest fomesafen rate tested (1120 g ai ha−1). The populations with a high frequency of ΔG210-homozygous survivors, and those with individuals harboring ΔG210 + G399A mutations, exhibited high potential for cross-resistance to other PPO herbicides. The new PPO–herbicide chemistries (saflufenacil, trifludimoxazin) generally controlled the PPO-resistant populations.

Highlights

The commercialization of genetically modified crops resistant to the highly effective, non-selective herbicide glyphosate has greatly impacted weed management
protoporphyrinogen IX oxidase (PPO)-inhibitor herbicides stop the oxidation of protoporphyrinogen IX into protoporphyrin IX, which leads to accumulation of protoporphyrinogen IX
The PPO enzyme exists in two forms in plants; PPO1 is located in the chloroplast, whereas PPO2 is in the mitochondria and, in a few species, in the chloroplast [18,19]

Summary

Introduction

The commercialization of genetically modified crops resistant to the highly effective, non-selective herbicide glyphosate has greatly impacted weed management. Relying on a single herbicide exerted tremendous selection pressure on weed populations, resulting in the evolution of many glyphosate-resistant weed species, including Amaranthus spp. In at least ten cases, a single A. palmeri population carries multiple resistance to ALS herbicides and glyphosate [6,10,11,12]. Herbicides inhibiting protoporphyrinogen oxidase (PPO, EC 1.3.3.4) have been used extensively to control ALS- and glyphosate-resistant A. palmeri populations. By inhibiting this enzyme, PPO-inhibitor herbicides stop the oxidation of protoporphyrinogen IX into protoporphyrin IX, which leads to accumulation of protoporphyrinogen IX. The PPO enzyme exists in two forms in plants; PPO1 is located in the chloroplast, whereas PPO2 is in the mitochondria and, in a few species, in the chloroplast [18,19]

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