scholarly journals Target-Site Resistances to ALS and PPO Inhibitors Are Linked in Waterhemp (Amaranthus tuberculatus)

Weed Science ◽  
2016 ◽  
Vol 65 (1) ◽  
pp. 4-8 ◽  
Author(s):  
Patrick J. Tranel ◽  
Chenxi Wu ◽  
Ahmed Sadeque
Keyword(s):  
Resistance Mechanism ◽  
Acetolactate Synthase ◽  
Resistance Mechanisms ◽  
Target Site ◽  
Recurrent Parent ◽  
Common Waterhemp ◽  
Independent Assortment ◽  
Resistance Evolution ◽  
Amaranthus Tuberculatus ◽  
Molecular Marker Analysis

It is generally expected that, in the case of multiple herbicide resistance, different resistance mechanisms within a weed will follow Mendel’s law of independent assortment. Research was conducted to investigate anecdotal observations suggesting that target site–based resistances to inhibitors of acetolactate synthase (ALS) and protoporphyrinogen oxidase (PPO) did not follow independent assortment in common waterhemp. Cosegregation of the two resistances was observed in backcross lines (population sensitive to both herbicides as recurrent parent). Specifically, whereas 52% of backcross plants were resistant to a PPO inhibitor, this percentage increased to 92% when the backcross plants were preselected for resistance to an ALS inhibitor. Molecular marker analysis confirmed that the corresponding genes (ALSandPPX2) were genetically linked. When data from all plants analyzed were pooled, the genetic distance between the two genes was calculated to be 7.5 cM. The two genes were found to be about 195 kb apart in the recently published grain amaranth genome, explaining the observed genetic linkage. There is likely enough recombination that occurs between the linked genes to prevent the linkage from having significant implications in terms of resistance evolution. Nevertheless, documentation of the happenstance linkage between target-site genes for resistance to ALS and PPO inhibitors in waterhemp is a reminder that one should not assume distinct resistance mechanism will independently assort.

Molecular confirmation of resistance to PPO inhibitors in Amaranthus tuberculatus and Amaranthus palmeri, and isolation of the G399A PPO2 substitution in A. palmeri

2020 ◽  
pp. 1-7
Author(s):  
Jacob S. Montgomery ◽  
Darci A. Giacomini ◽  
Patrick J. Tranel
Keyword(s):  
Goodness Of Fit ◽  
Resistance Mechanism ◽  
Amino Acid Position ◽  
Resistance Mechanisms ◽  
Palmer Amaranth ◽  
Target Site ◽  
Coding Region ◽  
Common Waterhemp ◽  
Growing Seasons ◽  
Target Site Resistance

Abstract During the 2017 to 2019 growing seasons, samples of waterhemp and Palmer amaranth that had reportedly survived field-rate applications of protoporphyrinogen oxidase (PPO)–inhibiting herbicides were collected from the American Midwest and tested for target-site mutations known at the time to confer resistance. Target-site resistance was identified in nearly all (135 of 145) tested common waterhemp populations but in only 8 of 13 Palmer amaranth populations. Follow-up research on one population of Palmer amaranth (W-8), which tested negative for all such mutations, confirmed it was resistant to lactofen, with a magnitude of resistance comparable to that conferred by the ΔG210 PPO2 mutation. Gene sequences from both isoforms of PPO (PPO1 and PPO2) were compared between W-8 and known PPO inhibitor–sensitive sequence. A glycine-to-alanine substitution at the 399th amino acid position (G399A) of PPO2, recently identified to reduce target-site herbicide sensitivity, was observed in a subset of resistant W-8 plants. Because no missense mutation completely delimited resistant and sensitive sequences, we initially suspected the presence of a secondary, non-target-site resistance mechanism in this population. To isolate G399A, a segregating F2 population was produced and screened with a delimiting rate of lactofen. χ2 goodness-of-fit analysis of dead/alive ratings indicated single-locus inheritance of resistance in the F2 population, and molecular markers for the W-8 parental PPO2 coding region co-segregated tightly, but not perfectly, with resistance. More research is needed to fully characterize Palmer amaranth PPO inhibitor–resistance mechanisms, which appear to be more diverse than those found in common waterhemp.

Target-Site Resistance Mechanisms to Tribenuron-methyl and Cross-resistance Patterns to ALS-inhibiting Herbicides of Catchweed Bedstraw (Galium aparine) with Different ALS Mutations

Weed Science ◽  
2018 ◽  
Vol 67 (2) ◽  
pp. 183-188 ◽  
Author(s):  
Wei Deng ◽  
Yingjie Di ◽  
Jingxuan Cai ◽  
Yueyang Chen ◽  
Shuzhong Yuan
Keyword(s):  
Acetolactate Synthase ◽  
Resistance Mechanisms ◽  
Target Site ◽  
Cross Resistance ◽  
Susceptible Population ◽  
Resistance Evolution ◽  
Galium Aparine ◽  
Resistance Patterns ◽  
Target Site Resistance ◽  
Tribenuron Methyl

AbstractCatchweed bedstraw (Galium aparine L.) is a problematic dicot weed that occurs in major winter wheat (Triticum aestivum L.) fields in China. Tribenuron-methyl has been widely used to control broadleaf weeds since 1988 in China. However, overuse has led to the resistance evolution of G. aparine to tribenuron-methyl. In this study, 20 G. aparine populations collected from Shandong and Henan provinces were used to determine tribenuron-methyl resistance and target-site resistance mechanisms. In dose–response experiments, 12 G. aparine populations showed different resistance levels (2.92 to 842.41-fold) to tribenuron-methyl compared with the susceptible population. Five different acetolactate synthase (ALS) mutations (Pro-197-Leu, Pro-197-Ser, Pro-197-His, Asp-376-Glu, and Trp-574-Leu) were detected in different resistant populations. Individuals heterozygous for Pro-197-Ser and Trp-574-Leu mutations were also observed in a resistant population (HN6). In addition, pHB4 (Pro-197-Ser), pHB7 (Pro-197-His), pHB8 (Pro-197-Leu), pHB5 (Asp-376-Glu), and pHB3 (Trp-574-Leu) subpopulations individually homozygous for specific ALS mutations were generated to evaluate the cross-resistance to ALS-inhibiting herbicides. The pHB4, pHB7, pHB8, pHB5, and pHB3 subpopulations all were resistant to sulfonylurea, pyrazosulfuron-ethyl, triazolopyrimidine, flumetsulam, sulfonylamino-carbonyl-triazolinone, flucarbazone-sodium, pyrimidinyl thiobenzoate, pyribenzoxim, and the imidazolinone imazethapyr. These results indicated the diversity of the resistance-conferring ALS mutations in G. aparine, and all these mutations resulted in broad cross-resistance to five kinds of ALS-inhibiting herbicides.

scholarly journals Survey of glyphosate-, atrazine- and lactofen-resistance mechanisms in Ohio waterhemp (Amaranthus tuberculatus) populations

Weed Science ◽  
2019 ◽  
Vol 67 (3) ◽  
pp. 296-302 ◽  
Author(s):  
Brent P. Murphy ◽  
Alvaro S. Larran ◽  
Bruce Ackley ◽  
Mark M. Loux ◽  
Patrick J. Tranel
Keyword(s):  
Gene Amplification ◽  
Herbicide Resistance ◽  
Crop Production ◽  
Resistance Mechanism ◽  
Population Level ◽  
Resistance Mechanisms ◽  
Amaranthus Retroflexus ◽  
Management Options ◽  
Common Waterhemp ◽  
Amaranthus Tuberculatus

AbstractHerbicide resistance within key driver weeds, such as common waterhemp [Amaranthus tuberculatus (Moq.) Sauer var. rudis (Sauer) Costea and Tardif ], constrains available management options for crop production. Routine surveillance for herbicide resistance provides a mechanism to monitor the development and spread of resistant populations over time. Furthermore, the identification and quantification of resistance mechanisms at the population level can provide information that helps growers develop effective management plans. Populations of Amaranthus spp., including A. tuberculatus, redroot pigweed (Amaranthus retroflexus L.), and Palmer amaranth (Amaranthus palmeri S. Watson), were collected from 51 fields in Ohio during the 2016 growing season. Twenty-four A. tuberculatus populations were screened for resistance to the herbicides lactofen, atrazine, and glyphosate. Phenotypically resistant plants were further investigated to determine the frequency of known resistance mechanisms. Resistance to lactofen was infrequently observed throughout the populations, with 8 of 22 populations exhibiting resistant plants. Within those eight resistant populations, the ΔG210 resistance mechanism was observed in 17 of 30 phenotypically resistant plants, and the remainder lacked all known resistance mechanisms. Resistance to atrazine was observed in 12 of 15 populations; however, a target-site resistance mechanism was not observed in these populations. Resistance to glyphosate was observed in all populations. Gene amplification was the predominant glyphosate-resistance mechanism (147 of 322 plants) in the evaluated populations. The Pro-106-Ser mutation was identified in 24 plants, half of which also possessed gene amplification. In this study, molecular screening generally underestimated the phenotypically observed resistance. Continued mechanism discovery and marker development is required for improved detection of herbicide resistance through molecular assays.

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

Weed Science ◽  
2017 ◽  
Vol 66 (2) ◽  
pp. 149-158 ◽  
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.

scholarly journals A high diversity of mechanisms endows ALS-inhibiting herbicide resistance in the invasive common ragweed (Ambrosia artemisiifolia L.)

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ingvild Loubet ◽  
Laëtitia Caddoux ◽  
Séverine Fontaine ◽  
Séverine Michel ◽  
Fanny Pernin ◽  
...  
Keyword(s):  
Resistance Mechanism ◽  
Resistance Management ◽  
Genotyping By Sequencing ◽  
Ambrosia Artemisiifolia ◽  
Target Site ◽  
Major Type ◽  
Common Ragweed ◽  
Resistance Evolution ◽  
Arable Weed ◽  
Target Site Resistance

AbstractAmbrosia artemisiifolia L. (common ragweed) is a globally invasive, allergenic, troublesome arable weed. ALS-inhibiting herbicides are broadly used in Europe to control ragweed in agricultural fields. Recently, ineffective treatments were reported in France. Target site resistance (TSR), the only resistance mechanism described so far for ragweed, was sought using high-throughput genotyping-by-sequencing in 213 field populations randomly sampled based on ragweed presence. Additionally, non-target site resistance (NTSR) was sought and its prevalence compared with that of TSR in 43 additional field populations where ALS inhibitor failure was reported, using herbicide sensitivity bioassay coupled with ALS gene Sanger sequencing. Resistance was identified in 46 populations and multiple, independent resistance evolution demonstrated across France. We revealed an unsuspected diversity of ALS alleles underlying resistance (9 amino-acid substitutions involved in TSR detected across 24 populations). Remarkably, NTSR was ragweed major type of resistance to ALS inhibitors. NTSR was present in 70.5% of the resistant plants and 74.1% of the fields harbouring resistance. A variety of NTSR mechanisms endowing different resistance patterns evolved across populations. Our study provides novel data on ragweed resistance to herbicides, and emphasises that local resistance management is as important as mitigating gene flow from populations where resistance has arisen.

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.

Distribution and validation of genotypic and phenotypic glyphosate and PPO-nhibitor resistance in Palmer amaranth (Amaranthus palmeri) from southwestern Nebraska

2020 ◽  
pp. 1-12 ◽  
Author(s):  
Maxwel C Oliveira ◽  
Darci A Giacomini ◽  
Nikola Arsenijevic ◽  
Gustavo Vieira ◽  
Patrick J Tranel ◽  
...  
Keyword(s):  
Cluster Analysis ◽  
Gene Amplification ◽  
Cropping Systems ◽  
Resistance Mechanism ◽  
Geographic Area ◽  
Glyphosate Resistance ◽  
Resistance Mechanisms ◽  
Palmer Amaranth ◽  
Resistance Evolution ◽  
Inhibitor Resistance

Abstract Failure to control Palmer amaranth with glyphosate and protoporphyrinogen IX oxidase (PPO)-inhibitor herbicides was reported across southwestern Nebraska in 2017. The objectives of this study were to 1) confirm and 2) validate glyphosate and PPO-inhibitor (fomesafen and lactofen) resistance in 51 Palmer amaranth accessions from southwestern Nebraska using genotypic and whole-plant phenotypic assay correlations and cluster analysis, and 3) determine which agronomic practices might be influencing glyphosate resistance in Palmer amaranth accessions in that location. Based on genotypic assay, 88% of 51 accessions contained at least one individual with amplification (>2 copies) of the 5-enolypyruvyl-shikimate-3-phosphate synthase (EPSPS) gene, which confers glyphosate resistance; and/or a mutation in the PPX2 gene, either ΔG210 or R128G, which endows PPO-inhibitor resistance in Palmer amaranth. Cluster analysis and high correlation (0.83) between genotypic and phenotypic assays demonstrated that EPSPS gene amplification is the main glyphosate resistance mechanism in Palmer amaranth accessions from southwestern Nebraska. In contrast, there was poor association between genotypic and phenotypic responses for PPO-inhibitor resistance, which was attributed to segregation for PPO-inhibitor resistance within these accessions and/or the methodology that was adopted herein. Genotypic assays can expedite the process of confirming known glyphosate and PPO-inhibitor resistance mechanisms in Palmer amaranth from southwestern Nebraska and other locations. Phenotypic assays are also a robust method for confirming glyphosate resistance but not necessarily PPO-inhibitor resistance in Palmer amaranth. Moreover, random forest analysis of glyphosate resistance in Palmer amaranth indicated that EPSPS gene amplification, county, and current and previous crops are the main factors influencing glyphosate resistance within that geographic area. Most glyphosate-susceptible Palmer amaranth accessions were found in a few counties in areas with high crop diversity. Results presented here confirm the spread of glyphosate resistance and PPO-inhibitor resistance in Palmer amaranth accessions from southwestern Nebraska and demonstrate that less diverse cropping systems are an important driver of herbicide resistance evolution in Palmer amaranth.

Acetolactate Synthase Resistance in a Common Waterhemp (Amaranthus rudis) Population

1997 ◽  
Vol 11 (1) ◽  
pp. 13-18 ◽  
Author(s):  
John R. R. Hinz ◽  
Micheal D. K. Owen
Keyword(s):  
Plant Material ◽  
Resistance Mechanism ◽  
Acetolactate Synthase ◽  
Grain Amaranth ◽  
Common Waterhemp ◽  
Resistant Species ◽  
Whole Plant ◽  
Amaranthus Rudis ◽  
Inhibitor Resistance ◽  
Als Inhibitor

Research was initiated to determine (a) whether a common waterhemp population was resistant to acetolactate synthase (ALS) inhibiting herbicides, (b) the percentage of the population that was ALS-inhibitor resistant, (c) the resistance mechanism, and (d) the effectiveness of a whole plant assay to detect ALS-inhibitor resistance. ALS-inhibitor resistance was confirmed in a common waterhemp population near Davis City, IA. The Davis City common waterhemp population was cross resistant to both imidazolinone and sulfonylurea herbicides, but not to lactofen. Approximately 10% of the Davis City common waterhemp population was sensitive to a rate of imazaquin 4 times the normal field rate. Davis City common waterhemp isolated ALS was much less sensitive to imazaquin and primisulfuron inhibition than was grain amaranth or an ALS-sensitive common waterhemp isolated ALS. Imazaquin I50values were 366.4 and 3.4 μM for ALS isolated from Davis City common waterhemp and grain amaranth, respectively. Primisulfuron I50values were 3.6 and 0.007 μM for ALS isolated from Davis City common waterhemp and grain amaranth, respectively. A whole plant ALS assay was developed that allowed for much more rapid detection of an ALS-resistant species and used less plant material than a conventional ALS assay.

scholarly journals Some approaches to new antibacterial agents

2007 ◽  
Vol 79 (12) ◽  
pp. 2143-2153 ◽  
Author(s):  
John B. Bremner
Keyword(s):  
Bacterial Resistance ◽  
Efflux Pump ◽  
Transmembrane Protein ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Target Site ◽  
Resistant Bacteria ◽  
General Strategy ◽  
Dual Action ◽  
Hybrid Drugs

Bacteria use a number of resistance mechanisms to counter the antibacterial challenge, and one of these is the expression of transmembrane protein-based efflux pumps which can pump out antibacterials from within the cells, thus lowering the antibacterial concentration to nonlethal levels. For example, in S. aureus, the NorA pump can pump out the antibacterial alkaloid berberine and ciprofloxacin. One general strategy to reduce the health threat of resistant bacteria is to block a major bacterial resistance mechanism at the same time as interfering with another bacterial pathway or target site. New developments of this approach in the context of dual-action prodrugs and dual-action (or hybrid) drugs in which one action is targeted at blocking the NorA efflux pump and the second action at an alternative bacterial target site (or sites) for the antibacterial action are discussed. The compounds are based on a combination of 2-aryl-5-nitro-1H-indole derivatives (as the NorA efflux pump blocking component) and derivatives of berberine. General design principles, syntheses, antibacterial testing, and preliminary work on modes of action studies are discussed.

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.

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