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

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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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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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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A Statewide Survey of PPO-Inhibitor Resistance and the Prevalent Target-Site Mechanisms in Palmer amaranth (Amaranthus palmeri) Accessions from Arkansas

Weed Science ◽

10.1017/wsc.2017.68 ◽

2017 ◽

Vol 66 (2) ◽

pp. 149-158 ◽

Cited By ~ 24

Author(s):

Vijay K. Varanasi ◽

Chad Brabham ◽

Jason K. Norsworthy ◽

Haozhen Nie ◽

Bryan G. Young ◽

...

Keyword(s):

Resistance Mechanism ◽

Acetolactate Synthase ◽

Resistance Mechanisms ◽

Palmer Amaranth ◽

Target Site ◽

Evolution Of Resistance ◽

Target Site Resistance ◽

Novel Target ◽

Als Inhibitors ◽

Inhibitor Resistance

Palmer amaranth is one of the most problematic weeds in the midsouthern United States, and the evolution of resistance to protoporphyrinogen oxidase (PPO) inhibitors in biotypes already resistant to glyphosate and acetolactate synthase (ALS) inhibitors is a major cause of concern to soybean and cotton growers in these states. A late-season weed-escape survey was conducted in the major row crop–producing counties (29 counties) to determine the severity of PPO-inhibitor resistance in Arkansas. A total of 227 Palmer amaranth accessions were sprayed with fomesafen at 395 g ha−1to identify putative resistant plants. A TaqMan qPCR assay was used to confirm the presence of the ΔG210 codon deletion or the R128G/M (homologous to R98 mutation in common ragweed) target-site resistance mechanisms in thePPX2gene. Out of the 227 accessions screened, 44 were completely controlled with fomesafen, and 16 had only one or two severely injured plants (≥98% mortality) when compared with the 1986 susceptible check (100% mortality). The remaining 167 accessions were genotypically screened, and 82 (49%) accessions were found to harbor the ΔG210 deletion in thePPX2gene. The R128G was observed in 47 (28%) out of the 167 accessions screened. The mutation R128M, on the other hand was rare, found in only three accessions. About 13% of the accessions were segregating for both the ΔG210 and R128G mutations. Sixteen percent of the tested accessions had mortality ratings <90% and did not test positive for the ΔG210 or the R128G/M resistance mechanisms, indicating that a novel target or non–target site resistance mechanism is likely. Overall, PPO inhibitor–resistant Palmer amaranth is widespread in Arkansas, and the ΔG210 resistance mechanism is especially dominant in the northeast corridor, while the R128G mutation is more prevalent in counties near Memphis, TN.

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Non-Target-Site Resistance Mechanisms Endow Multiple Herbicide Resistance to Five Mechanisms of Action in Conyza bonariensis

Journal of Agricultural and Food Chemistry ◽

10.1021/acs.jafc.1c04279 ◽

2021 ◽

Author(s):

Candelario Palma-Bautista ◽

José G. Vázquez-García ◽

José Alfredo Domínguez-Valenzuela ◽

Kassio Ferreira Mendes ◽

Ricardo Alcántara de la Cruz ◽

...

Keyword(s):

Herbicide Resistance ◽

Resistance Mechanisms ◽

Mechanisms Of Action ◽

Target Site ◽

Conyza Bonariensis ◽

Target Site Resistance ◽

Multiple Herbicide Resistance

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Functional Genomics Analysis of Horseweed (Conyza canadensis) with Special Reference to the Evolution of Non–Target-Site Glyphosate Resistance

Weed Science ◽

10.1614/ws-d-09-00037.1 ◽

2010 ◽

Vol 58 (2) ◽

pp. 109-117 ◽

Cited By ~ 48

Author(s):

Joshua S. Yuan ◽

Laura L. G. Abercrombie ◽

Yongwei Cao ◽

Matthew D. Halfhill ◽

Xin Zhou ◽

...

Keyword(s):

Functional Genomics ◽

Molecular Mechanisms ◽

Glyphosate Resistance ◽

Resistance Mechanisms ◽

Target Site ◽

Environmentally Benign ◽

Conyza Canadensis ◽

Target Site Resistance ◽

Weedy Species ◽

Heterologous Microarray

The evolution of glyphosate resistance in weedy species places an environmentally benign herbicide in peril. The first report of a dicot plant with evolved glyphosate resistance was horseweed, which occurred in 2001. Since then, several species have evolved glyphosate resistance and genomic information about nontarget resistance mechanisms in any of them ranges from none to little. Here, we report a study combining iGentifier transcriptome analysis, cDNA sequencing, and a heterologous microarray analysis to explore potential molecular and transcriptomic mechanisms of nontarget glyphosate resistance of horseweed. The results indicate that similar molecular mechanisms might exist for nontarget herbicide resistance across multiple resistant plants from different locations, even though resistance among these resistant plants likely evolved independently and available evidence suggests resistance has evolved at least four separate times. In addition, both the microarray and sequence analyses identified non–target-site resistance candidate genes for follow-on functional genomics analysis.

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Target and Non–target site Mechanisms Confer Resistance to Glyphosate in Canadian Accessions ofConyza canadensis

Weed Science ◽

10.1017/wsc.2017.69 ◽

2017 ◽

Vol 66 (2) ◽

pp. 234-245 ◽

Cited By ~ 8

Author(s):

Eric R. Page ◽

Christopher M. Grainger ◽

Martin Laforest ◽

Robert E. Nurse ◽

Istvan Rajcan ◽

...

Keyword(s):

Ssr Markers ◽

Resistance Mechanisms ◽

Target Site ◽

Conyza Canadensis ◽

Weed Species ◽

Target Site Resistance ◽

Selection For ◽

Simple Sequence ◽

Growing Region ◽

Selection Of

Glyphosate-resistant populations ofConyza canadensishave been spreading at a rapid rate in Ontario, Canada, since first being documented in 2010. Determining the genetic relationship among existing Ontario populations is necessary to understand the spread and selection of the resistant biotypes. The objectives of this study were to: (1) characterize the genetic variation ofC. canadensisaccessions from the province of Ontario using simple sequence repeat (SSR) markers and (2) investigate the molecular mechanism (s) conferring resistance in these accessions. Ninety-eightC. canadensisaccessions were genotyped using 8 SSR markers. Germinable accessions were challenged with glyphosate to determine their dose response, and the sequences of 5-enolpyruvylshikimate-3-phosphate synthase genes 1 and 2 were obtained. Results indicate that a majority of glyphosate-resistant accessions from Ontario possessed a proline to serine substitution at position 106, which has previously been reported to confer glyphosate resistance in other crop and weed species. Accessions possessing this substitution demonstrated notably higher levels of resistance than non–target site resistant (NTSR) accessions from within or outside the growing region and were observed to form a subpopulation genetically distinct from geographically proximate glyphosate-susceptible and NTSR accessions. Although it is unclear whether other non–target site resistance mechanisms are contributing to the levels of resistance observed in target-site resistant accessions, these results indicate that, at a minimum, selection for Pro-106-Ser has occurred in addition to selection for non–target site resistance and has significantly enhanced the levels of resistance to glyphosate inC. canadensisaccessions from Ontario.

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Multiple Herbicide-Resistant Weeds and Non-target Site Resistance Mechanisms: A Global Challenge for Food Production

10.3389/978-2-88971-908-2 ◽

2021 ◽

Keyword(s):

Food Production ◽

Resistance Mechanisms ◽

Target Site ◽

Herbicide Resistant ◽

Global Challenge ◽

Target Site Resistance

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Evolution of target and non-target based multiple herbicide resistance in a single Palmer amaranth (Amaranthus palmeri) population from Kansas

Weed Technology ◽

10.1017/wet.2020.32 ◽

2020 ◽

Vol 34 (3) ◽

pp. 447-453

Author(s):

Sushila Chaudhari ◽

Vijay K. Varanasi ◽

Sridevi Nakka ◽

Prasanta C. Bhowmik ◽

Curtis R. Thompson ◽

...

Keyword(s):

Resistance Mechanism ◽

Acetolactate Synthase ◽

Palmer Amaranth ◽

Target Site ◽

Epsp Synthase ◽

High Incidence ◽

Evolution Of Resistance ◽

Target Site Resistance ◽

Herbicide Atrazine ◽

Sites Of Action

AbstractThe evolution of resistance to multiple herbicides in Palmer amaranth is a major challenge for its management. In this study, a Palmer amaranth population from Hutchinson, Kansas (HMR), was characterized for resistance to inhibitors of photosystem II (PSII) (e.g., atrazine), acetolactate synthase (ALS) (e.g., chlorsulfuron), and EPSP synthase (EPSPS) (e.g., glyphosate), and this resistance was investigated. About 100 HMR plants were treated with field-recommended doses (1×) of atrazine, chlorsulfuron, and glyphosate, separately along with Hutchinson multiple-herbicide (atrazine, chlorsulfuron, and glyphosate)–susceptible (HMS) Palmer amaranth as control. The mechanism of resistance to these herbicides was investigated by sequencing or amplifying the psbA, ALS, and EPSPS genes, the molecular targets of atrazine, chlorsulfuron, and glyphosate, respectively. Fifty-two percent of plants survived a 1× (2,240 g ai ha−1) atrazine application with no known psbA gene mutation, indicating the predominance of a non–target site resistance mechanism to this herbicide. Forty-two percent of plants survived a 1× (18 g ai ha−1) dose of chlorsulfuron with proline197serine, proline197threonine, proline197alanine, and proline197asparagine, or tryptophan574leucine mutations in the ALS gene. About 40% of the plants survived a 1× (840 g ae ha−1) dose of glyphosate with no known mutations in the EPSPS gene. Quantitative PCR results revealed increased EPSPS copy number (50 to 140) as the mechanism of glyphosate resistance in the survivors. The most important finding of this study was the evolution of resistance to at least two sites of action (SOAs) (~50% of plants) and to all three herbicides due to target site as well as non–target site mechanisms. The high incidence of individual plants with resistance to multiple SOAs poses a challenge for effective management of this weed.

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Physiological assessment of non–target site restistance in multiple-resistant junglerice (Echinochloa colona)

Weed Science ◽

10.1017/wsc.2019.52 ◽

2019 ◽

Vol 67 (6) ◽

pp. 622-632 ◽

Cited By ~ 1

Author(s):

Christopher E. Rouse ◽

Nilda Roma-Burgos ◽

Bianca Assis Barbosa Martins

Keyword(s):

Management Practices ◽

Enzyme Inhibitors ◽

Treatment Resistance ◽

Target Site ◽

Metabolic Enzyme ◽

Herbicide Resistant ◽

Whole Plant ◽

Detoxification Mechanism ◽

Target Site Resistance ◽

Resistance To Herbicides

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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