Herbicide-resistance mechanisms: gene amplification is not just for glyphosate

2017 ◽  
Vol 73 (11) ◽  
pp. 2225-2226 ◽  
Author(s):  
Patrick J Tranel
Keyword(s):  
Gene Amplification ◽  
Herbicide Resistance ◽  
Resistance Mechanisms

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.

Gene Amplification and Herbicide Resistance

2017 ◽  
pp. 173-184
Author(s):  
Mithila Jugulam ◽  
Karthik Putta ◽  
Vijay K. Varanasi ◽  
Dal-Hoe Koo
Keyword(s):  
Gene Amplification ◽  
Herbicide Resistance

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.

scholarly journals Widespread occurrence of both metabolic and target-site herbicide resistance mechanisms inLolium rigidumpopulations

2015 ◽  
Vol 72 (2) ◽  
pp. 255-263 ◽  
Author(s):  
Heping Han ◽  
Qin Yu ◽  
Mechelle J Owen ◽  
Gregory R Cawthray ◽  
Stephen B Powles
Keyword(s):  
Herbicide Resistance ◽  
Resistance Mechanisms ◽  
Target Site ◽  
Widespread Occurrence

scholarly journals Mechanisms of evolved herbicide resistance

2020 ◽  
Vol 295 (30) ◽  
pp. 10307-10330 ◽  
Author(s):  
Todd A. Gaines ◽  
Stephen O. Duke ◽  
Sarah Morran ◽  
Carlos A. G. Rigon ◽  
Patrick J. Tranel ◽  
...  
Keyword(s):  
Herbicide Resistance ◽  
Cytochromes P450 ◽  
Management Strategies ◽  
Resistance Management ◽  
Gene Families ◽  
Resistance Mechanisms ◽  
Weed Species ◽  
Individual Level ◽  
Large Gene ◽  
Aryl Acylamidase

The widely successful use of synthetic herbicides over the past 70 years has imposed strong and widespread selection pressure, leading to the evolution of herbicide resistance in hundreds of weed species. Both target-site resistance (TSR) and nontarget-site resistance (NTSR) mechanisms have evolved to most herbicide classes. TSR often involves mutations in genes encoding the protein targets of herbicides, affecting the binding of the herbicide either at or near catalytic domains or in regions affecting access to them. Most of these mutations are nonsynonymous SNPs, but polymorphisms in more than one codon or entire codon deletions have also evolved. Some herbicides bind multiple proteins, making the evolution of TSR mechanisms more difficult. Increased amounts of protein target, by increased gene expression or by gene duplication, are an important, albeit less common, TSR mechanism. NTSR mechanisms include reduced absorption or translocation and increased sequestration or metabolic degradation. The mechanisms that can contribute to NTSR are complex and often involve genes that are members of large gene families. For example, enzymes involved in herbicide metabolism–based resistances include cytochromes P450, GSH S-transferases, glucosyl and other transferases, aryl acylamidase, and others. Both TSR and NTSR mechanisms can combine at the individual level to produce higher resistance levels. The vast array of herbicide-resistance mechanisms for generalist (NTSR) and specialist (TSR and some NTSR) adaptations that have evolved over a few decades illustrate the evolutionary resilience of weed populations to extreme selection pressures. These evolutionary processes drive herbicide and herbicide-resistant crop development and resistance management strategies.

Dominant expression of a gene amplification-related herbicide resistance in medicago cell hybrids

1988 ◽  
Vol 7 (3) ◽  
pp. 158-161 ◽  
Author(s):  
Maria Deak ◽  
Gunter Donn ◽  
Attila Feher ◽  
Denes Dudits
Keyword(s):  
Gene Amplification ◽  
Herbicide Resistance ◽  
Cell Hybrids

scholarly journals Evolution of MET and NRAS gene amplification as acquired resistance mechanisms in EGFR mutant NSCLC

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
T. L. Peters ◽  
T. Patil ◽  
A. T. Le ◽  
K. D. Davies ◽  
P. M. Brzeskiewicz ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Gene Amplification ◽  
Treatment Options ◽  
Acquired Resistance ◽  
Mek Inhibitor ◽  
Resistance Mechanisms ◽  
Molecular Testing ◽  
Egfr Inhibitor ◽  
Lung Cancer Patients ◽  
Egfr Mutant

AbstractEGFR mutant non-small cell lung cancer patients' disease demonstrates remarkable responses to EGFR-targeted therapy, but inevitably they succumb to acquired resistance, which can be complex and difficult to treat. Analyzing acquired resistance through broad molecular testing is crucial to understanding the resistance mechanisms and developing new treatment options. We performed diverse clinical testing on a patient with successive stages of acquired resistance, first to an EGFR inhibitor with MET gene amplification and then subsequently to a combination EGFR and MET targeted therapies. A patient-derived cell line obtained at the time of disease progression was used to identify NRAS gene amplification as an additional driver of drug resistance to combination EGFR/MET therapies. Analysis of downstream signaling revealed extracellular signal-related kinase activation that could only be eliminated by trametinib treatment, while Akt activation could be modulated by various combinations of MET, EGFR, and PI3K inhibitors. The combination of an EGFR inhibitor with a MEK inhibitor was identified as a possible treatment option to overcome drug resistance related to NRAS gene amplification.

scholarly journals Extrachromosomal circular DNA-based amplification and transmission of herbicide resistance in crop weedAmaranthus palmeri

2018 ◽  
Vol 115 (13) ◽  
pp. 3332-3337 ◽  
Author(s):  
Dal-Hoe Koo ◽  
William T. Molin ◽  
Christopher A. Saski ◽  
Jiming Jiang ◽  
Karthik Putta ◽  
...  
Keyword(s):  
Gene Amplification ◽  
Herbicide Resistance ◽  
Germ Cells ◽  
Gene Copy Number ◽  
Gene Copy ◽  
Circular Dna ◽  
Dna Structures ◽  
Meiotic Chromosomes ◽  
Extrachromosomal Elements ◽  
Mitosis And Meiosis

Gene amplification has been observed in many bacteria and eukaryotes as a response to various selective pressures, such as antibiotics, cytotoxic drugs, pesticides, herbicides, and other stressful environmental conditions. An increase in gene copy number is often found as extrachromosomal elements that usually contain autonomously replicating extrachromosomal circular DNA molecules (eccDNAs).Amaranthus palmeri, a crop weed, can develop herbicide resistance to glyphosate [N-(phosphonomethyl) glycine] by amplification of the 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) gene, the molecular target of glyphosate. However, biological questions regarding the source of the amplifiedEPSPS, the nature of the amplified DNA structures, and mechanisms responsible for maintaining this gene amplification in cells and their inheritance remain unknown. Here, we report that amplifiedEPSPScopies in glyphosate-resistant (GR)A. palmeriare present in the form of eccDNAs with various conformations. The eccDNAs are transmitted during cell division in mitosis and meiosis to the soma and germ cells and the progeny by an as yet unknown mechanism of tethering to mitotic and meiotic chromosomes. We propose that eccDNAs are one of the components of McClintock’s postulated innate systems [McClintock B (1978)Stadler Genetics Symposium] that can rapidly produce soma variation, amplifyEPSPSgenes in the sporophyte that are transmitted to germ cells, and modulate rapid glyphosate resistance through genome plasticity and adaptive evolution.

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