Mechanism of Resistance to S-metolachlor in Palmer amaranth.

Gulab Rangani,Nilda Roma-Burgos,Matheus Noguera,Lariza Benedetti,Reiofeli Salas-Perez

doi:10.3389/fpls.2021.652581

Abstract

Herbicides are major tools for effective weed management. The evolution of resistance to herbicides in weedy species, especially contributed by non-target-site-based resistance (NTSR) is a worrisome issue in crop production globally. Glyphosate-resistant Palmer amaranth (Amaranthus palmeri) is one of the extremely difficult weeds in southern US crop production. In this study, we present the level and molecular basis of resistance to the chloroacetamide herbicide, S-metolachlor, in six field-evolved A. palmeri populations that had survivors at the recommended field-dose (1.1 kg ai ha−1). These samples were collected in 2014 and 2015. The level of resistance was determined in dose-response assays. The effective dose for 50% control (ED50) of the susceptible population was 27 g ai ha−1, whereas the ED50 of the resistant populations ranged from 88 to 785 g ai ha−1. Therefore, A. palmeri resistance to S-metolachlor evolved in Arkansas as early as 2014. Metabolic-inhibitor and molecular assays indicated NTSR in these populations, mainly driven by GSTs. To understand the mechanism of resistance, selected candidate genes were analyzed in leaves and roots of survivors (with 1 × S-metolachlor). Expression analysis of the candidate genes showed that the primary site of S-metolachlor detoxification in A. palmeri is in the roots. Two GST genes, ApGSTU19 and ApGSTF8 were constitutively highly expressed in roots of all plants across all resistant populations tested. The expression of both GSTs increased further in survivors after treatment with S-metolachlor. The induction level of ApGSTF2 and ApGSTF2like by S-metolachlor differed among resistant populations. Overall, higher expression of ApGSTU19, ApGSTF8, ApGSTF2, and ApGSTF2like, which would lead to higher GST activity in roots, was strongly associated with the resistant phenotype. Phylogenetic relationship and analysis of substrate binding site of candidate genes suggested functional similarities with known metolachlor-detoxifying GSTs, effecting metabolic resistance to S-metolachlor in A. palmeri. Resistance is achieved by elevated baseline expression of these genes and further induction by S-metolachlor in resistant plants.

Highlights

The evolution of resistance in response to intensive herbicide selection pressure in weedy species is a worldwide problem in crop production
To verify that GST enzymes were involved in resistance to Smetolachlor, we tested the effect of S-metolachlor on seedling growth of A. palmeri in the presence and absence of GST inhibitor, NBD-Cl
VLCFA-inhibiting herbicides are used to control a broad spectrum of broadleaf and grass weeds in various crops

Summary

Introduction

The evolution of resistance in response to intensive herbicide selection pressure in weedy species is a worldwide problem in crop production. S-metolachlor is a member of the chloroacetamide chemical family under Group 15 of the Weed Science Society of America (WSSA) classification system. Group 15 herbicides are soil-active and inhibit seedling root and shoot growth by blocking the formation of very long chain fatty acids (VLCFA, site-of-action), acting even before the susceptible grass or broadleaf weeds emerge. S-metolachlor is typically used preemergence in corn (Zea mays L.), cotton (Gossypium hirsutum L.), soybean [Glycine max (L.) Merr] and many other crops, including turfgrass, for the control of grasses and small-seeded broadleaf weeds. Among the primary weeds controlled by S-metolachlor are Amaranthus species. In the USA, S-metolachlor is the third largest volume of herbicide active ingredient used, following glyphosate and atrazine (Atwood and Paisley-Jones, 2017)

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