Molecular and Genomic Mechanisms of Non-Target-Site Herbicide Resistance

2009 ◽  
pp. 149-161 ◽  
Author(s):  
Jun Hu ◽  
Patrick J. Tranel ◽  
C. Neal Stewart ◽  
Joshua S. Yuan
Keyword(s):  
Herbicide Resistance ◽  
Target Site

Investigating the resistance levels and mechanisms to penoxsulam and cyhalofop-butyl in barnyardgrass (Echinochloa crus-galli) from Ningxia province, China

Weed Science ◽  
2021 ◽  
pp. 1-25
Author(s):  
Qian Yang ◽  
Xia Yang ◽  
Zichang Zhang ◽  
Jieping Wang ◽  
Weiguo Fu ◽  
...  
Keyword(s):  
Herbicide Resistance ◽  
Molecular Mechanisms ◽  
Acetolactate Synthase ◽  
Rice Fields ◽  
Target Site ◽  
Herbicide Resistant ◽  
Susceptible Populations ◽  
High Level ◽  
Als Inhibitor ◽  
Encoding Genes

Abstract Barnyardgrass (Echinochloa crus-galli) is a noxious grass weed which infests rice fields and causes huge crop yield losses. In this study, we collected twelve E. crus-galli populations from rice fields of Ningxia province in China and investigated the resistance levels to acetolactate synthase (ALS) inhibitor penoxsulam and acetyl-CoA carboxylase (ACCase) inhibitor cyhalofop-butyl. The results showed that eight populations exhibited resistance to penoxsulam and four populations evolved resistance to cyhalofop-butyl. Moreover, all of the four cyhalofop-butyl-resistant populations (NX3, NX4, NX6 and NX7) displayed multiple-herbicide-resistance (MHR) to both penoxsulam and cyhalofop-butyl. The alternative herbicides bispyribac-sodium, metamifop and fenoxaprop-P-ethyl cannot effectively control the MHR plants. To characterize the molecular mechanisms of resistance, we amplified and sequenced the target-site encoding genes in resistant and susceptible populations. Partial sequences of three ALS genes and six ACCase genes were examined. A Trp-574-Leu mutation was detected in EcALS1 and EcALS3 in two high-level (65.84- and 59.30-fold) penoxsulam-resistant populations NX2 and NX10, respectively. In addition, one copy (EcACC4) of ACCase genes encodes a truncated aberrant protein due to a frameshift mutation in E. crus-galli populations. None of amino acid substitutions that are known to confer herbicide resistance were detected in ALS and ACCase genes of MHR populations. Our study reveals the widespread of multiple-herbicide resistant E. crus-galli populations at Ningxia province of China that exhibit resistance to several ALS and ACCase inhibitors. Non-target-site based mechanisms are likely to be involved in E. crus-galli resistance to the herbicides, at least in four MHR populations.

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).

scholarly journals Standing genetic variation fuels rapid evolution of herbicide resistance in blackgrass

2021 ◽  
Author(s):  
Sonja Kersten ◽  
Jiyang Chang ◽  
Christian D Huber ◽  
Yoav Voichek ◽  
Christa Lanz ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Herbicide Resistance ◽  
Large Scale ◽  
De Novo ◽  
Bulked Segregant Analysis ◽  
Target Site ◽  
Temperate Climate ◽  
Minor Role ◽  
Standing Variation ◽  
Target Site Resistance

Repeated herbicide applications exert enormous selection on blackgrass (Alopecurus myosuroides), a major weed in cereal crops of the temperate climate zone including Europe. This inadvertent large-scale experiment gives us the opportunity to look into the underlying genetic mechanisms and evolutionary processes of rapid adaptation, which can occur both through mutations in the direct targets of herbicides and through changes in other, often metabolic, pathways, known as non-target-site resistance. How much either type of adaptation relies on de novo mutations versus pre-existing standing variation is important for developing strategies to manage herbicide resistance. We generated a chromosome-level reference genome for A. myosuroides for population genomic studies of herbicide resistance and genome-wide diversity across Europe in this species. Bulked-segregant analysis evidenced that non-target-site resistance has a complex genetic architecture. Through empirical data and simulations, we showed that, despite its simple genetics, target-site resistance mainly results from standing genetic variation, with only a minor role for de novo mutations.

Multiple herbicide resistance in California Italian ryegrass (Lolium perenne ssp. multiflorum): characterization of ALS-inhibiting herbicide resistance

Weed Science ◽  
2019 ◽  
Vol 67 (3) ◽  
pp. 273-280 ◽  
Author(s):  
Parsa Tehranchian ◽  
Vijay K. Nandula ◽  
Maor Matzrafi ◽  
Marie Jasieniuk
Keyword(s):  
Lolium Perenne ◽  
Herbicide Resistance ◽  
Resistance Mechanism ◽  
Acetolactate Synthase ◽  
Target Site ◽  
Italian Ryegrass ◽  
Resistance Level ◽  
Als Inhibitors ◽  
Inhibitor Resistance ◽  
Als Inhibitor

AbstractMultiple resistance to glyphosate, sethoxydim, and paraquat was previously confirmed in two Italian ryegrass [Lolium perenne L. ssp. multiflorum (Lam.) Husnot] populations, MR1 and MR2, in northern California. Preliminary greenhouse studies revealed that both populations were also resistant to imazamox and mesosulfuron, both of which are acetolactate synthase (ALS)-inhibiting herbicides. In this study, three subpopulations, MR1-A (from seed of MR1 plants that survived a 16X rate of sethoxydim), MR1-P (from seed of MR1 plants that survived a 2X rate of paraquat), and MR2 (from seed of MR2 plants that survived a 16X rate of sethoxydim), were investigated to determine the resistance level to imazamox and mesosulfuron, evaluate other herbicide options for the control of these multiple resistant L. perenne ssp. multiflorum, and characterize the underlying ALS-inhibitor resistance mechanism(s). Based on LD50 values, the MR1-A, MR1-P, and MR2 subpopulations were 38-, 29-, 8-fold and 36-, 64-, and 3-fold less sensitive to imazamox and mesosulfuron, respectively, relative to the susceptible (Sus) population. Only MR1-P and MR2 plants were cross-resistant to rimsulfuron, whereas both MR1 subpopulations were cross-resistant to imazethapyr. Pinoxaden (ACCase inhibitor [phenylpyrazoline 'DEN']) only controlled MR2 and Sus plants at the labeled field rate. However, all plants were effectively controlled (>99%) with the labeled field rate of glufosinate. Based on I50 values, MR1-A, MR-P, and MR2 plants were 712-, 1,104-, and 3-fold and 10-, 18-, and 5-fold less responsive to mesosulfuron and imazamox, respectively, than the Sus plants. Sequence alignment of the ALS gene of resistant plants revealed a missense single-nucleotide polymorphism resulting in a Trp-574-Leu substitution in MR1-A and MR1-P plants, heterozygous in both, but not in the MR2 plants. An additional homozygous substitution, Asp-376-Glu, was identified in the MR1-A plants. Addition of malathion or piperonyl butoxide did not alter the efficacy of mesosulfuron on MR2 plants. In addition, the presence of 2,4-D had no effect on the response of mesosulfuron on the MR2 and Sus. These results suggest an altered target site is the mechanism of resistance to ALS inhibitors in MR1-A and MR1-P plants, whereas a non–target site based resistance apparatus is present in the MR2 plants.

Basis for Herbicide Resistance in Canadian Populations of Wild Oat (Avena fatua)

Weed Science ◽  
2012 ◽  
Vol 60 (1) ◽  
pp. 10-18 ◽  
Author(s):  
Hugh J. Beckie ◽  
Suzanne I. Warwick ◽  
Connie A. Sauder
Keyword(s):  
Herbicide Resistance ◽  
Economic Effects ◽  
Target Site ◽  
Northern Great Plains ◽  
Western Canada ◽  
Wild Oat ◽  
Site Mutation ◽  
P450 Monooxygenase ◽  
Als Inhibitors ◽  
Als Inhibitor

Wild oat is the second-most abundant, but most economically important, weed across the Canadian Prairies of western Canada. Despite the serious economic effects of resistance to acetyl-CoA carboxylase (ACC) or acetolactate synthase (ALS) inhibitors or both in this weed throughout the Northern Great Plains of North America, little research has examined the basis for herbicide resistance. We investigated target-site and nontarget-site mechanisms conferring ACC- and ALS-inhibitor resistance in 16 wild oat populations from across western Canada (four ACC-inhibitor resistant, four ALS-inhibitor resistant, and eight ACC- and ALS-inhibitor resistant). TheACC1mutations were found in 8 of the 12 ACC inhibitor-resistant populations. The Ile1781Leu mutation was detected in three populations, the Trp2027Cys and Asp2078Gly mutations were in two populations each, and the Trp1999Cys, Ile2041Asn, Cys2088Arg, and Gly2096Ser substitutions were in one population each. Three populations had twoACC1mutations. Only 2 of the 12 ALS inhibitor-resistant populations had anALStarget-site mutation—Ser653Thr and Ser653Asn substitutions. This is the first global report ofALStarget-site mutations inAvenaspp. and four previously undocumentedACC1mutations in wild oat. Based on these molecular analyses, seedlings of five ACC + ALS inhibitor-resistant populations (one with anACC1mutation; four with noACCorALSmutations) were treated with malathion, a known cytochrome P450 monooxygenase inhibitor, followed by application of one of four ACC- or ALS-inhibiting herbicides. Malathion treatment often resulted in control or suppression of these populations, suggesting involvement of this enzyme system in contributing to resistance to both ACC and ALS inhibitors.

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 Target-Site Mutations Conferring Herbicide Resistance

Plants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 382 ◽  
Author(s):  
Brent P. Murphy ◽  
Patrick J. Tranel
Keyword(s):  
Amino Acid ◽  
Herbicide Resistance ◽  
Target Site ◽  
Single Amino Acid ◽  
Cross Resistance ◽  
Target Sites ◽  
Resistance Patterns ◽  
Experimental Approaches ◽  
Sites Of Action ◽  
Multiple Amino Acid

Mutations conferring evolved herbicide resistance in weeds are known in nine different herbicide sites of action. This review summarizes recently reported resistance-conferring mutations for each of these nine target sites. One emerging trend is an increase in reports of multiple mutations, including multiple amino acid changes at the glyphosate target site, as well as mutations involving two nucleotide changes at a single amino acid codon. Standard reference sequences are suggested for target sites for which standards do not already exist. We also discuss experimental approaches for investigating cross-resistance patterns and for investigating fitness costs of specific target-site mutations.

Acetolactate synthase inhibitor-resistant stinkweed (Thlaspi arvense L.) in Alberta

2007 ◽  
Vol 87 (4) ◽  
pp. 965-972 ◽  
Author(s):  
H. J. Beckie ◽  
L. M. Hall ◽  
F. J. Tardif ◽  
G. Séguin-Swartz
Keyword(s):  
Herbicide Resistance ◽  
Dominant Gene ◽  
Acetolactate Synthase ◽  
Target Site ◽  
Cross Resistance ◽  
Resistance Pattern ◽  
Site Mutation ◽  
Thlaspi Arvense ◽  
Synthase Inhibitor ◽  
Als Inhibitor

Two stinkweed populations from southern and central Alberta were not controlled by acetolactate synthase (ALS)-inhibiting herbicides in 2000. This study reports on their cross-resistance to ALS-inhibiting herbicides, molecular basis of resistance, and inheritance of resistance. Both putative herbicide-resistant biotypes responded similarly to increasing doses of the herbicides. The biotypes were highly resistant to ethametsulfuron and exhibited a low level of resistance to metsulfuron and imazethapyr. However, both biotypes were not resistant to florasulam, a triazolopyrimidine ALS inhibitor, or sulfometuron, a non-selective sulfonylurea ALS inhibitor. The cross-resistance pattern was consistent with the confirmed target-site mutation. Sequence analysis of the ALS gene detected a Pro197Leu mutation in both biotypes. Similar to many other ALS inhibitor-resistant weed biotypes, resistance was conferred by a single dominant gene. This study confirms the first global occurrence of herbicide resistance in this species. Key words: ALS-inhibitor resistance, ALS sequence, herbicide resistance, target-site mutation

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