Physiological and Molecular Characterization of Hydroxyphenylpyruvate Dioxygenase (HPPD)-inhibitor Resistance in Palmer Amaranth (Amaranthus palmeri S.Wats.).

Sridevi Nakka,Mithila Jugulam,Amar S Godar,Prashant S Wani,Jeroen Roelofs,Dallas E Peterson,Curtis R Thompson

doi:10.3389/fpls.2017.00555

Sridevi Nakka, Mithila Jugulam + Show 5 more

Open Access

https://doi.org/10.3389/fpls.2017.00555

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Abstract

Herbicides that inhibit hydroxyphenylpyruvate dioxygenase (HPPD) such as mesotrione are widely used to control a broad spectrum of weeds in agriculture. Amaranthus palmeri is an economically troublesome weed throughout the United States. The first case of evolution of resistance to HPPD-inhibiting herbicides in A. palmeri was documented in Kansas (KS) and later in Nebraska (NE). The objective of this study was to investigate the mechansim of HPPD-inhibitor (mesotrione) resistance in A. palmeri. Dose response analysis revealed that this population (KSR) was 10–18 times more resistant than their sensitive counterparts (MSS or KSS). Absorbtion and translocation analysis of [14C] mesotrione suggested that these mechanisms were not involved in the resistance in A. palmeri. Importantly, mesotrione (>90%) was detoxified markedly faster in the resistant populations (KSR and NER), within 24 hours after treatment (HAT) compared to sensitive plants (MSS, KSS, or NER). However, at 48 HAT all populations metabolized the mesotrione, suggesting additional factors may contribute to this resistance. Further evaluation of mesotrione-resistant A. palmeri did not reveal any specific resistance-conferring mutations nor amplification of HPPD gene, the molecular target of mesotrione. However, the resistant populations showed 4- to 12-fold increase in HPPD gene expression. This increase in HPPD transcript levels was accompanied by increased HPPD protein expression. The significant aspects of this research include: the mesotrione resistance in A. palmeri is conferred primarily by rapid detoxification (non-target-site based) of mesotrione; additionally, increased HPPD gene expression (target-site based) also contributes to the resistance mechanism in the evolution of herbicide resistance in this naturally occurring weed species.

Highlights

Mesotrione is a synthetic triketone herbicide chemically known as 2-[4-(methylsulfonyl)-2-nitrobenzoyl]-1,3-cyclohexanedione and biochemically inhibits 4-hydroxyphenylpyruvate dioxygenase (HPPD)
The HPPD-inhibitor-resistant and -susceptible Palmer amaranth populations were derived from different locations
We found a variation in the level of resistance to mesotrione at individual plant level in all populations, especially the KSR2 (Figure 1A)

Summary

Introduction

Mesotrione is a synthetic triketone herbicide chemically known as 2-[4-(methylsulfonyl)-2-nitrobenzoyl]-1,3-cyclohexanedione and biochemically inhibits 4-hydroxyphenylpyruvate dioxygenase (HPPD) This enzyme is important in the catabolism of tyrosine and anabolism of plastoquinones, tocopherols, and subsequently carotenoid biosynthesis (Beaudegnies et al, 2009). HPPD-inhibitors are broadly classified into three chemical families: isoxazoles (e.g., isoxaflutole and pyrasulfotole), pyrazolones (e.g., topramezone), and triketones (e.g., mesotrione and tembotrione) depending on the chemical structure and properties (Lee et al, 1998). Upon treatment with these herbicides, susceptible plants exhibit characteristic bleaching symptoms as a result of loss of carotenoid synthesis and eventually leading to lipid peroxidation of cell membranes. It is important to preserve the effectiveness and extend the use of these herbicides as no herbicides with new modes of action have been introduced in the last 20 years (Duke, 2012), and new herbicide-resistant traits are being stacked in crops to control weeds

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