Abstract

Extensive acceptance of glyphosate-resistant (GR) row crops coupled with the simultaneous increase in glyphosate usage has sped the evolution of glyphosate resistance in economically important weeds. GR Amaranthus palmeri populations are widespread across the state with some exhibiting multiple resistance to acetolactate synthase (ALS) inhibiting herbicides such as pyrithiobac. A GR and ALS inhibitor-resistant accession was also resistant to the protoporphyrinogen oxidase (PPO) inhibiting herbicide fomesafen. The PPO inhibitor resistance profile and multiple herbicide resistance mechanisms in this accession were investigated. In addition to fomesafen, resistance to postemergence applications of acifluorfen, lactofen, carfentrazone, and sulfentrazone was confirmed. There was no resistance to preemergence application of fomesafen, flumioxazin, or oxyfluorfen. Molecular analysis of the ALS gene indicated the presence of point mutations leading to single nucleotide substitutions at codons 197, 377, 574, and 653, resulting in proline-to-serine, arginine-to-glutamine, tryptophan-to-leucine, and serine-to-asparagine replacements, respectively. The resistant accession contained up to 87-fold more copies of the EPSPS gene compared to a susceptible accession. A mutation leading to a deletion of glycine at codon 210 (ΔG210) of PPO2 gene was also detected. These results indicate that the mechanism of resistance in the Palmer amaranth accession is target-site based, i.e., altered target site for ALS and PPO inhibitor resistance and gene amplification for glyphosate resistance.

Highlights

  • The collective attributes of glyphosate herbicide, from its systemic action to its nonselective, wide range of postemergence activity, has contributed to its broad appeal throughout the world in both crop and noncrop lands since its commercialization in 1974

  • GR Amaranthus palmeri populations are widespread across the state with some exhibiting multiple resistance to acetolactate synthase (ALS) inhibiting herbicides such as pyrithiobac

  • These results indicate that the mechanism of resistance in the Palmer amaranth accession is target-site based, i.e., altered target site for ALS and protoporphyrinogen oxidase (PPO) inhibitor resistance and gene amplification for glyphosate resistance

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Summary

Introduction

The collective attributes of glyphosate herbicide, from its systemic action to its nonselective, wide range of postemergence activity, has contributed to its broad appeal throughout the world in both crop and noncrop lands since its commercialization in 1974. The widespread adoption of GR crops around the world has led to overuse of the herbicide and reduced crop rotation, which resulted in the evolution of several GR weed biotypes. As of May 2020, GR populations have been reported for 48 weed species worldwide [1], including Amaranthus palmeri (S.) Wat. Before the commercialization of GR crops, acetolactate synthase (ALS) inhibiting herbicides were used extensively for weed management in crop and noncrop areas. A major downside to the widespread use of ALS inhibitors has been the rapid and extensive evolution of resistance in several grasses and broadleaf weed populations across the world. As of May 2020, 165 weed species have been documented to be resistant to one or more ALS inhibitors [1]. Among these resistant weed species are several Amaranthus spp. including A. palmeri

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