scholarly journals Impact of a Novel W2027L Mutation and Non-Target Site Resistance on Acetyl-CoA Carboxylase-Inhibiting Herbicides in a French Lolium multiflorum Population

Genes ◽  
2021 ◽  
Vol 12 (11) ◽  
pp. 1838
Author(s):  
Shiv Shankhar Kaundun ◽  
Joe Downes ◽  
Lucy Victoria Jackson ◽  
Sarah-Jane Hutchings ◽  
Eddie Mcindoe
Keyword(s):  
Lolium Multiflorum ◽  
Restriction Enzymes ◽  
Target Site ◽  
Cereal Crops ◽  
Acetyl Coa Carboxylase ◽  
Wild Type ◽  
Resistance Mutations ◽  
Acetyl Coa ◽  
Pcr Product ◽  
Target Site Resistance

Herbicides that inhibit acetyl-CoA carboxylase (ACCase) are among the few remaining options for the post-emergence control of Lolium species in small grain cereal crops. Here, we determined the mechanism of resistance to ACCase herbicides in a Lolium multiflorum population (HGR) from France. A combined biological and molecular approach detected a novel W2027L ACCase mutation that affects aryloxyphenoxypropionate (FOP) but not cyclohexanedione (DIM) or phenylpyraxoline (DEN) subclasses of ACCase herbicides. Both the wild-type tryptophan and mutant leucine 2027-ACCase alleles could be positively detected in a single DNA-based-derived polymorphic amplified cleaved sequence (dPACS) assay that contained the targeted PCR product and a cocktail of two discriminating restriction enzymes. Additionally, we identified three well-characterised I1781L, I2041T, and D2078G ACCase target site resistance mutations as well as non-target site resistance in HGR. The non-target site component endowed high levels of resistance to FOP herbicides whilst partially impacting on the efficacy of pinoxaden and cycloxydim. This study adequately assessed the contribution of the W2027L mutation and non-target site mechanism in conferring resistance to ACCase herbicides in HGR. It also highlights the versatility and robustness of the dPACS method to simultaneously identify different resistance-causing alleles at a single ACCase codon.

scholarly journals Impact of a Novel W2027L Mutation And Non-Target Site Resistance On Acetyl-CoA Carboxylase Herbicides In a French Lolium Multiflorum Population

2021 ◽  
Author(s):  
Shiv Shankhar Kaundun ◽  
Joe Downes ◽  
Lucy Victoria Jackson ◽  
Sarah-Jane Hutchings ◽  
Eddie Mcindoe
Keyword(s):  
Lolium Multiflorum ◽  
Restriction Enzymes ◽  
Target Site ◽  
Cereal Crops ◽  
Acetyl Coa Carboxylase ◽  
Wild Type ◽  
Resistance Mutations ◽  
Acetyl Coa ◽  
Pcr Product ◽  
Target Site Resistance

Abstract Herbicides that inhibit acetyl-CoA carboxylase (ACCase) are among the few remaining options for the post-emergence control of Lolium species in small grain cereal crops. Here we have determined the mechanism of resistance to ACCase herbicides in a Lolium multiflorum population (HGR) from France. A combined biological and molecular approach detected a novel W2027L ACCase mutation that affects aryloxyphenoxypropionate (FOP) but not cyclohexanedione (DIM) or phenylpyraxoline (DEN) subclasses of ACCase herbicides. Both the wild type tryptophan and mutant leucine 2027-ACCase alleles could be positively detected in a single DNA-based derived Polymorphic amplified cleaved sequence (dPACS) assay that contained the targeted PCR product and a cocktail of two discriminating restriction enzymes. Additionally, we have identified three well-characterised I1781L, I2041T and D2078G target site resistance mutations as well as non-target site resistance in HGR. The non-target site component endowed high levels of resistance to FOP herbicides whilst partially impacting on the efficacy of pinoxaden and cycloxydim. This study adequately assessed the contribution of the W2027L mutation and non-target site mechanism in conferring resistance to ACCase herbicides in HGR. It also highlights the versatility and robustness of the dPACS method to simultaneously identify different resistance-causing alleles at a single ACCase codon.

scholarly journals A Novel W1999S Mutation and Non-Target Site Resistance Impact on Acetyl-CoA Carboxylase Inhibiting Herbicides to Varying Degrees in a UK Lolium multiflorum Population

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e58012 ◽  
Author(s):  
Shiv Shankhar Kaundun ◽  
Geraldine C. Bailly ◽  
Richard P. Dale ◽  
Sarah-Jane Hutchings ◽  
Eddie McIndoe
Keyword(s):  
Lolium Multiflorum ◽  
Target Site ◽  
Acetyl Coa Carboxylase ◽  
Acetyl Coa ◽  
Target Site Resistance

scholarly journals First Detection and Characterization of Cross- and Multiple Resistance to Acetyl-CoA Carboxylase (ACCase)- and Acetolactate Synthase (ALS)-Inhibiting Herbicides in Black-Grass (Alopecurus myosuroides) and Italian Ryegrass (Lolium multiflorum) Populations from Ireland

Agriculture ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1272
Author(s):  
Vijaya Bhaskar Alwarnaidu Vijayarajan ◽  
Patrick D Forristal ◽  
Sarah K Cook ◽  
David Schilder ◽  
Jimmy Staples ◽  
...  
Keyword(s):  
Lolium Multiflorum ◽  
Acetolactate Synthase ◽  
Target Site ◽  
Italian Ryegrass ◽  
Integrated Weed Management ◽  
Multiple Resistance ◽  
Acetyl Coa Carboxylase ◽  
Acetyl Coa ◽  
Alopecurus Myosuroides ◽  
Target Site Resistance

Understanding the resistance spectrum and underlying genetic mechanisms is critical for managing herbicide-resistant populations. In this study, resistance to acetyl CoA carboxylase (ACCase) and acetolactate synthase (ALS) inhibitors was investigated in four suspected resistant populations of Alopecurus myosuroides (ALOMY-001 to ALOMY-004) and Lolium multiflorum (LOLMU-001 to LOLMU-004), collected from cereal production fields in Ireland. Glasshouse assays with three ALOMY-active herbicides [propaquizafop, cycloxydim (ACCase) and mesosulfuron + iodosulfuron (ALS)] or five LOLMU-active herbicides [pinoxaden, propaquizafop, cycloxydim (ACCase) and mesosulfuron + iodosulfuron, pyroxsulam (ALS)], and target-site resistance mechanism studies, based on pyrosequencing, were carried out in each of those populations. For A. myosuroides, Ile-1781-Leu ACCase mutation contributed to propaquizafop and cycloxydim resistance (shoot dry weight GR50 resistance factor (RF) = 7.5–35.5) in all ALOMY populations, and the independent Pro-197-Thr or Pro-197-Ser ALS mutation contributed to mesosulfuron + iodosulfuron resistance (RF = 3.6–6.6), in ALOMY-002 to ALOMY-004. Most of the analyzed plants for these mutations were homo/heterozygous combinations or only heterozygous. For L. multiflorum, phenotypic resistance to mesosulfuron + iodosulfuron (RF = 11.9–14.6) and pyroxsulam (RF = 2.3–3.1) was noted in all LOLMU populations, but the Pro-197-Gln or Pro-197-Leu ALS mutation (mostly in homozygous status) was identified in LOLMU-001, LOLMU-002 and LOLMU-004 only. Additionally, despite no known ACCase mutations in any LOLMU populations, LOLMU-002 survived pinoxaden and propaquizafop application (RF = 3.4 or 1.3), and LOLMU-003 survived pinoxaden (RF = 2.3), suggesting the possibility of non-target-site resistance mechanisms for ACCase and/or ALS resistance in these populations. Different resistance levels, as evidenced by a reduction in growth as dose increased above field rates in ALOMY and LOLMU, were due to variations in mutation rate and the level of heterozygosity, resulting in an overall resistance rating of low to moderate. This is the first study confirming cross- and multiple resistance to ACCase- and ALS-inhibiting herbicides, highlighting that resistance monitoring in A. myosuroides and L. multiflorum in Ireland is critical, and the adoption of integrated weed management strategies (chemical and non-chemical/cultural strategies) is essential.

scholarly journals Acetyl-CoA Carboxylase 2−/− Mutant Mice are Protected against Fatty Liver under High-fat, High-carbohydrate Dietary and de Novo Lipogenic Conditions

2012 ◽  
Vol 287 (15) ◽  
pp. 12578-12588 ◽  
Author(s):  
Lutfi Abu-Elheiga ◽  
Hongmei Wu ◽  
Ziwei Gu ◽  
Rubin Bressler ◽  
Salih J. Wakil
Keyword(s):  
Fatty Liver ◽  
De Novo ◽  
Mutant Mice ◽  
Acetyl Coa Carboxylase ◽  
Wild Type ◽  
High Fat ◽  
Acetyl Coa ◽  
High Carbohydrate ◽  
Ppar Γ ◽  
Hepatic Fat

Hepatic fat accumulation resulting from increased de novo fatty acid synthesis leads to hepatic steatosis and hepatic insulin resistance. We have shown previously that acetyl-CoA carboxylase 2 (Acc2−/−) mutant mice, when fed a high-fat (HF) or high-fat, high-carbohydrate (HFHC) diet, are protected against diet-induced obesity and maintained whole body and hepatic insulin sensitivity. To determine the effect of an ACC2 deletion on hepatic fat metabolism, we studied the regulation of the enzymes involved in the lipogenic pathway under Western HFHC dietary and de novo lipogenic conditions. After completing the HFHC regimen, Acc2−/− mutant mice were found to have lower body weight, smaller epididymal fat pads, lower blood levels of nonesterified fatty acids and triglycerides, and higher hepatic cholesterol than wild-type mice. Significant up-regulation of lipogenic enzymes and an elevation in hepatic peroxisome proliferator-activated receptor-γ (PPAR-γ) protein were found in Acc2−/− mutant mice under de novo lipogenic conditions. The increase in lipogenic enzyme levels was accompanied by up-regulation of the transcription factors, sterol regulatory element-binding proteins 1 and 2, and carbohydrate response element-binding protein. In contrast, hepatic levels of the PPAR-γ and PPAR-α proteins were significantly lower in the Acc2−/− mutant mice fed an HFHC diet. When compared with wild-type mice fed the same diet, Acc2−/− mutant mice exhibited a similar level of AKT but with a significant increase in pAKT. Hence, deleting ACC2 ameliorates the metabolic syndrome and protects against fatty liver despite increased de novo lipogenesis and dietary conditions known to induce obesity and diabetes.

scholarly journals Interaction of acetyl-CoA carboxylase enzyme inhibiting herbicides with auxin herbicides on ryegrass

2021 ◽  
Vol 51 (4) ◽  
Author(s):  
Rubens Antonio Polito ◽  
Larissa Pasqualotto ◽  
Rafael Dysarz ◽  
Rafaela Cinelli ◽  
Tamara Heck ◽  
...  
Keyword(s):  
Weed Control ◽  
Coenzyme A ◽  
Lolium Multiflorum ◽  
Antagonistic Effect ◽  
Acetyl Coa Carboxylase ◽  
Herbicide Application ◽  
Acetyl Coa ◽  
Antagonistic Interaction ◽  
Auxin Herbicides

ABSTRACT: This study aimed to evaluate the antagonistic effect of the mixture ofacetyl coenzyme-A carboxylase (ACCase) enzyme inhibiting herbicides and auxin herbicides in Lolium multiflorum and to determine mechanisms to mitigate this possible effect. The first experiments were conducted by associating the herbicide clethodim (108 g a.i. ha−1), quizalofop-p-ethyl (54 g a.i. ha−1), and clethodim + quizalofop-p-ethyl (108+54 g a.i. ha−1) with 2,4-D (1005 g a.e. ha−1) or triclopyr (720 g a.e. ha−1), in addition to the sole application of the respective graminicides. Another experiment included clethodim (54; 81; 108; 162; 216 g a.i. ha−1), quizalofop-p-ethyl (27; 40.5; 54; 81; 108 g a.i. ha−1), and clethodim + quizalofop-p-ethyl (54+27; 81+40.5; 108+54; 162+81; 216+108 g a.i. ha−1) mixed with 2,4-D (1005 g a.e. ha−1), or triclopyr (720 g a.e. ha−1), in addition to the control treatments without herbicide application. In the second experiment, herbicides clethodim (108 g a.i. ha−1), quizalofop-p-ethyl (54 g a.i. ha−1), and clethodim + quizalofop-p-ethyl (108+54 g a.i. ha−1) in combination with the herbicides 2,4-D (1005 g a.e. ha−1) or triclopyr (720 g a.e. ha−1)had malathion (1000 g a.i. ha−1) or glyphosate (720 g a.e. ha−1) mixed, in addition to the sole applications of the graminicides. The herbicide clethodim + quizalofop-p-ethyl did not present an antagonistic interaction with the auxin herbicides, and obtained 85% weed control. To obtain control similar to the sole application of this graminicide, the dose of the herbicide clethodim needs to be increased by 20%. However, the mixture of the herbicide quizalofop-p-ethyl with 2,4-D and triclopyr affects the ryegrass control. The use of strategies that increase the absorption of ACCase herbicides or the inhibition of P450 enzymes are ways to mitigate the antagonistic effect caused by the association of the two auxin herbicides.

Acetyl-CoA Carboxylase-a Graminicide Target Site

1997 ◽  
Vol 50 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Derek Herbert ◽  
Kevin A. Walker ◽  
Lindsey J. Price ◽  
David J. Cole ◽  
Kenneth E. Pallett ◽  
...  
Keyword(s):  
Target Site ◽  
Acetyl Coa Carboxylase ◽  
Acetyl Coa
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