Segregation of non-target-site resistance to herbicides in multiple-resistantAlopecurus myosuroidesplants

AbstractHerbicide-resistant Echinochloa species are among the most problematic weeds in agricultural crops globally. Recurring herbicide selection pressure in the absence of diverse management practices has resulted in greater than 20% of sampled Echinochloa populations from rice (Oryza sativa L.) fields demonstrating multiple resistance to herbicides in Arkansas, USA. We assessed the resistance profile and potential mechanisms of resistance in a multiple herbicide–resistant junglerice [Echinochloa colona (L.) Link] (ECO-R) population. Whole-plant and laboratory bioassays were conducted to identify the potential mechanisms of non–target site resistance in this population. ECO-R was highly resistant to propanil (>37,800 g ha−1) and quinclorac (>17,920 g ha−1) and had elevated tolerance to cyhalofop (R/S = 1.9) and glufosinate (R/S = 1.2) compared to the susceptible standard. The addition of glufosinate (590 g ha−1) to cyhalofop (314 g ha−1), propanil (4,500 g ha−1), or quinclorac (560 g ha−1) controlled ECO-R 100%. However, cyhalofop applied with propanil (48% control) or quinclorac (15% control) was antagonistic. The application of the known metabolic enzyme inhibitors malathion, carbaryl, and piperonyl butoxide increased control of ECO-R with propanil (>75%) but not with other herbicides. Neither absorption nor translocation of [14C]cyhalofop or propanil was different between ECO-R and ECO-S. [14C]Quinclorac absorption was also similar between ECO-R and ECO-S; however, translocation of quinclorac into tissues above the treated leaf of ECO-R was >20% higher than that in ECO-S. The abundance of metabolites was higher (∼10%) in the treated leaves of ECO-R than in ECO-S beginning 48 h after treatment. The activity of β-cyanoalanine synthase, which detoxifies hydrogen cyanide, was not different between ECO-R and ECO-S following quinclorac treatment. Resistance to propanil was due to herbicide detoxification by metabolic enzymes. Resistance to quinclorac was due to a detoxification mechanism yet to be understood. The reduction in sensitivity to cyhalofop and glufosinate might be a secondary effect of the mechanisms conferring high resistance to propanil and quinclorac.

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Molecular Mechanisms of Herbicide Resistance

Weed Science ◽

10.1614/ws-d-13-00096.1 ◽

2015 ◽

Vol 63 (SP1) ◽

pp. 91-115 ◽

Cited By ~ 45

Author(s):

Christophe Délye ◽

Arnaud Duhoux ◽

Fanny Pernin ◽

Chance W. Riggins ◽

Patrick J. Tranel

Keyword(s):

Herbicide Resistance ◽

Molecular Mechanisms ◽

Target Site ◽

Target Protein ◽

Intrinsic Activity ◽

Evolutionary Adaptation ◽

Herbicide Binding ◽

Target Site Resistance ◽

Resistance To Herbicides ◽

Increased Activity

Resistance to herbicides occurs in weeds as the result of evolutionary adaptation (Jasieniuk et al. 1996). Basically, two types of mechanisms are involved in resistance (Beckie and Tardif 2012; Délye 2013). Target-site resistance (TSR) is caused by changes in the tridimensional structure of the herbicide target protein that decrease herbicide binding, or by increased activity (e.g., due to increased expression or increased intrinsic activity) of the target protein. Nontarget-site resistance (NTSR) is endowed by any mechanism not belonging to TSR, e.g., reduction in herbicide uptake or translocation in the plant, or enhanced herbicide detoxification (reviewed in Délye 2013; Yuan et al. 2007).

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Origin, mechanism and molecular basis of weed resistance to herbicides

Plant Protection Science ◽

10.17221/463-pps ◽

2010 ◽

Vol 40 (No. 4) ◽

pp. 151-168 ◽

Cited By ~ 2

Author(s):

D. Chodová ◽

J. Mikulka ◽

M. Kočová ◽

J. Salava

Keyword(s):

D1 Protein ◽

Acetolactate Synthase ◽

Target Site ◽

Gene Encoding ◽

Genetic Modifications ◽

The World ◽

Target Sites ◽

Target Site Resistance ◽

Resistance To Herbicides ◽

Weed Resistance

This review summarises information from the literature and experimental experience of the authors in research on weed resistance to herbicides. Factors conditioning the origin of resistance are described. The origin of resistant weeds to nine active ingredients with a different mode of action is presented chronologically, and the distribution of resistant weeds around the world outlined. The fundamental modes of action: reduction of the target site sensitivity, so-called "target site resistance", and the mode by which a herbicide is metabolised into inactive products, are listed. Function and genetic modifications of target sites of selected herbicides are described. Czech biotypes of resistant weeds with a mutation at codon 264 of the psbA gene encoding the D1 protein and at codon 574 of the acetolactate synthase gene are presented.

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Non-Target-Site Resistance to Herbicides: Recent Developments

Plants ◽

10.3390/plants8100417 ◽

2019 ◽

Vol 8 (10) ◽

pp. 417 ◽

Cited By ~ 10

Author(s):

Jugulam ◽

Shyam

Keyword(s):

Weed Management ◽

Management Strategies ◽

Target Site ◽

Cross Resistance ◽

Weed Species ◽

Physiological Processes ◽

Recent Developments ◽

Target Site Resistance ◽

Resistance To Herbicides ◽

Selection Of

Non-target-site resistance (NTSR) to herbicides in weeds can be conferred as a result of the alteration of one or more physiological processes, including herbicide absorption, translocation, sequestration, and metabolism. The mechanisms of NTSR are generally more complex to decipher than target-site resistance (TSR) and can impart cross-resistance to herbicides with different modes of action. Metabolism-based NTSR has been reported in many agriculturally important weeds, although reduced translocation and sequestration of herbicides has also been found in some weeds. This review focuses on summarizing the recent advances in our understanding of the physiological, biochemical, and molecular basis of NTSR mechanisms found in weed species. Further, the importance of examining the co-existence of TSR and NTSR for the same herbicide in the same weed species and influence of environmental conditions in the altering and selection of NTSR is also discussed. Knowledge of the prevalence of NTSR mechanisms and co-existing TSR and NTSR in weeds is crucial for designing sustainable weed management strategies to discourage the further evolution and selection of herbicide resistance in weeds.

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Weed resistance to herbicides

Acta herbologica ◽

10.5937/actaherb2002079v ◽

2020 ◽

Vol 29 (2) ◽

pp. 79-96

Author(s):

Sava Vrbničanin

Keyword(s):

Herbicide Resistance ◽

Amaranthus Retroflexus ◽

Ambrosia Artemisiifolia ◽

Target Site ◽

Weed Species ◽

Ps Ii ◽

Target Site Resistance ◽

Resistance To Herbicides ◽

Als Inhibitors ◽

Weed Resistance

Weed resistance to herbicides represents the acquired resistance of individuals to complete the life cycle and leave offspring in the conditions of extended exposure to the same herbicide, i.e. herbicides of the same mechanism of action to which they were sensitive at the beginning of the application. Based on the herbicide resistance mechanisms, all processes can be grouped as follows: target-site resistance, non-target-site resistance, cross-resistance and multiple-resistance. Currently, herbicide resistance has been reported in 514 cases (species x site of action) worldwide, in 262 weed species (152 dicotyledons, 110 monocotyledons). Many of those biotypes are resistant to als inhibitors, PS II inhibitors, EPSPS inhibitors and ACC-ase inhibitors. The higher degree of resistance to als inhibitors has been confirmed in the following weed species: Amaranthus retroflexus, Sorghum halepense, Ambrosia artemisiifolia and Helianthus annuus.

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Metabolism-Based Herbicide Resistance, the Major Threat Among the Non-Target Site Resistance Mechanisms

Outlooks on Pest Management ◽

10.1564/v31_aug_04 ◽

2020 ◽

Vol 31 (4) ◽

pp. 162-168

Author(s):

Carlos A. G. Rigon ◽

Todd A. Gaines ◽

Anita Küpper ◽

Franck E. Dayan

Keyword(s):

Herbicide Resistance ◽

Resistance Mechanisms ◽

Target Site ◽

Major Threat ◽

Evolution Of Resistance ◽

Target Site Resistance ◽

Metabolic Degradation ◽

Varied Chemical ◽

Resistance To Herbicides ◽

Global Food

Evolution of resistance to pesticides is a problem challenging the sustainability of global food production. Resistance to herbicides is driven by the intense selection pressure imparted by synthetic herbicides on which we rely to manage weeds. Target-site resistance (TSR) mechanisms involve changes to the herbicide target protein and provide resistance only to herbicides within a single mechanism of action. Non-target site resistance (NTSR) mechanisms reduce the quantity of herbicide reaching the target site and/or modify the herbicide. NTSR mechanisms include reduced absorption and/or translocation, increased sequestration, and enhanced metabolic degradation. Of these diverse mechanisms contributing to NTSR, metabolism-based herbicide resistance represents a major threat because it can impart resistance to herbicides from varied chemical classes across any number of mechanisms of action.

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