scholarly journals Origin, mechanism and molecular basis of weed resistance to herbicides

2010 ◽  
Vol 40 (No. 4) ◽  
pp. 151-168 ◽  
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.

scholarly journals Weed resistance to herbicides

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.

Controlling Herbicide-Resistant Annual Bluegrass (Poa annua) Phenotypes with Methiozolin

2017 ◽  
Vol 31 (3) ◽  
pp. 470-476 ◽  
Author(s):  
James T. Brosnan ◽  
Jose J. Vargas ◽  
Gregory K. Breeden ◽  
Sarah L. Boggess ◽  
Margaret A. Staton ◽  
...  
Keyword(s):  
Acetolactate Synthase ◽  
Target Site ◽  
Multiple Resistance ◽  
Herbicide Resistant ◽  
Annual Bluegrass ◽  
Microtubule Inhibitors ◽  
Effective Option ◽  
Target Site Resistance ◽  
Susceptible Control ◽  
Als Inhibitors

Methiozolin is an isoxazoline herbicide being investigated for selective POST annual bluegrass control in managed turfgrass. Research was conducted to evaluate methiozolin efficacy for controlling two annual bluegrass phenotypes with target-site resistance to photosystem II (PSII) or enolpyruvylshikimate-3-phosphate synthase (EPSPS)-inhibiting herbicides (i.e., glyphosate), as well as phenotypes with multiple resistance to microtubule and EPSPS or PSII and acetolactate synthase (ALS)-inhibiting herbicides. All resistant phenotypes were established in glasshouse culture along with a known herbicide-susceptible control and treated with methiozolin at 0, 125, 250, 500, 1000, 2000, 4000, or 8000 g ai ha−1. Methiozolin effectively controlled annual bluegrass with target-site resistance to inhibitors of EPSPS, PSII, as well as multiple resistance to EPSPS and microtubule inhibitors. Methiozolin rates required to reduce aboveground biomass of these resistant phenotypes 50% (GR50 values) were not significantly different from the susceptible control, ranging from 159 to 421 g ha−1. A phenotype with target-site resistance to PSII and ALS inhibitors was less sensitive to methiozolin (GR50=862 g ha−1) than a susceptible phenotype (GR50=423 g ha−1). Our findings indicate that methiozolin is an effective option for controlling select annual bluegrass phenotypes with target-site resistance to several herbicides.

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

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.

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

Weed Science ◽  
2019 ◽  
Vol 67 (6) ◽  
pp. 622-632 ◽  
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.

scholarly journals Molecular Mechanisms of Herbicide Resistance

Weed Science ◽  
2015 ◽  
Vol 63 (SP1) ◽  
pp. 91-115 ◽  
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).

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

Weed Research ◽  
2015 ◽  
Vol 55 (3) ◽  
pp. 298-308 ◽  
Author(s):  
M Rosenhauer ◽  
F G Felsenstein ◽  
H-P Piepho ◽  
M Höfer ◽  
J Petersen
Keyword(s):  
Target Site ◽  
Target Site Resistance ◽  
Resistance To Herbicides

scholarly journals Point Mutations as Main Resistance Mechanism Together With P450-Based Metabolism Confer Broad Resistance to Different ALS-Inhibiting Herbicides in Glebionis coronaria From Tunisia

2021 ◽  
Vol 12 ◽  
Author(s):  
Zeineb Hada ◽  
Yosra Menchari ◽  
Antonia M. Rojano-Delgado ◽  
Joel Torra ◽  
Julio Menéndez ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Dose Response ◽  
Resistance Mechanism ◽  
Point Mutations ◽  
Acetolactate Synthase ◽  
Target Site ◽  
Cross Resistance ◽  
P450 Monooxygenase ◽  
Target Site Resistance ◽  
Sites Of Action

Resistance to acetolactate synthase (ALS) inhibiting herbicides has recently been reported in Glebionis coronaria from wheat fields in northern Tunisia, where the weed is widespread. However, potential resistance mechanisms conferring resistance in these populations are unknown. The aim of this research was to study target-site resistance (TSR) and non-target-site resistance (NTSR) mechanisms present in two putative resistant (R) populations. Dose–response experiments, ALS enzyme activity assays, ALS gene sequencing, absorption and translocation experiments with radiolabeled herbicides, and metabolism experiments were carried out for this purpose. Whole plant trials confirmed high resistance levels to tribenuron and cross-resistance to florasulam and imazamox. ALS enzyme activity further confirmed cross-resistance to these three herbicides and also to bispyribac, but not to flucarbazone. Sequence analysis revealed the presence of amino acid substitutions in positions 197, 376, and 574 of the target enzyme. Among the NTSR mechanisms investigated, absorption or translocation did not contribute to resistance, while evidences of the presence of enhanced metabolism were provided. A pretreatment with the cytochrome P450 monooxygenase (P450) inhibitor malathion partially synergized with imazamox in post-emergence but not with tribenuron in dose–response experiments. Additionally, an imazamox hydroxyl metabolite was detected in both R populations in metabolism experiments, which disappeared with the pretreatment with malathion. This study confirms the evolution of cross-resistance to ALS inhibiting herbicides in G. coronaria from Tunisia through TSR and NTSR mechanisms. The presence of enhanced metabolism involving P450 is threatening the chemical management of this weed in Tunisian wheat fields, since it might confer cross-resistance to other sites of action.

scholarly journals Multiple-Herbicide Resistance in a 2,4-D–Resistant Waterhemp (Amaranthus tuberculatus) Population from Nebraska

Weed Science ◽  
2017 ◽  
Vol 65 (6) ◽  
pp. 743-754 ◽  
Author(s):  
Roberto J. Crespo ◽  
Ana B. Wingeyer ◽  
Greg R. Kruger ◽  
Chance W. Riggins ◽  
Patrick J. Tranel ◽  
...  
Keyword(s):  
D1 Protein ◽  
Acetolactate Synthase ◽  
Mechanisms Of Action ◽  
Target Site ◽  
Site Mutation ◽  
Auxin Receptor ◽  
Application Rates ◽  
Chlorimuron Ethyl ◽  
Als Inhibitors ◽  
Susceptible Populations

A 2,4-D-resistant tall waterhemp population (FS) from Nebraska was evaluated for resistance to other TIR1 auxin receptor herbicides and to herbicides having alternative mechanisms of action using greenhouse bioassays and genetic markers. Atrazine, imazethapyr, lactofen, mesotrione, glufosinate, and glyphosate were applied in a single-dose bioassay, and tissue was collected from marked plants for genetic analysis. The FS population was not injured by atrazine or by imazethapyr. Approximately 50% of the plants survived lactofen and were actively growing 28 d after treatment. The population was susceptible to mesotrione, glufosinate, and glyphosate. Ametryn, chlorimuron-ethyl, 2,4-D, aminocyclopyraclor, aminopyralid, and picloram were applied in dose–response studies. The FS population was sensitive to ametryn, and the Ser-264-Gly substitution in the D1 protein was not detected, suggesting the lack of response to atrazine is not due to a target-site mutation. The FS population exhibited less than 50% injury to chlorimuron-ethyl at application rates 20 times the labeled use rate. The Ser-653-Asn acetolactate synthase (ALS) substitution, which confers resistance to imidazolinone herbicides, was present in the FS population. However, this does not explain the lack of response to the sulfonylurea herbicide, chlorimuron-ethyl. Sequencing of a portion of thePPX2Lgene did not show the ΔG210 mutation that confers resistance to protoporphyrinogen oxidase–inhibiting herbicides, suggesting that other factors were responsible for waterhemp survival after lactofen application. The FS population was confirmed to be at least 30-fold resistant to 2,4-D relative to the susceptible populations. In addition, it was at least 3-fold less sensitive to aminopyralid and picloram, two other TIR1 auxin receptor herbicides, than the 2,4-D-susceptible populations were. These data indicated that the FS population contains both target and non–target site mechanisms conferring resistance to herbicides spanning at least three mechanisms of action: TIR1 auxin receptors, ALS inhibitors, and photosystem II inhibitors.

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