scholarly journals Dinitroaniline Herbicide Resistance and Mechanisms in Weeds

2021 ◽  
Vol 12 ◽  
Author(s):  
Jinyi Chen ◽  
Qin Yu ◽  
Eric Patterson ◽  
Chad Sayer ◽  
Stephen Powles
Keyword(s):  
Point Mutations ◽  
Resistance Mutation ◽  
Target Site ◽  
Lolium Rigidum ◽  
Resistance Mutations ◽  
Metabolic Resistance ◽  
P450 Gene ◽  
Helical Growth ◽  
Target Site Resistance ◽  
Dinitroaniline Herbicides

Dinitroanilines are microtubule inhibitors, targeting tubulin proteins in plants and protists. Dinitroaniline herbicides, such as trifluralin, pendimethalin and oryzalin, have been used as pre-emergence herbicides for weed control for decades. With widespread resistance to post-emergence herbicides in weeds, the use of pre-emergence herbicides such as dinitroanilines has increased, in part, due to relatively slow evolution of resistance in weeds to these herbicides. Target-site resistance (TSR) to dinitroaniline herbicides due to point mutations in α-tubulin genes has been confirmed in a few weedy plant species (e.g., Eleusine indica, Setaria viridis, and recently in Lolium rigidum). Of particular interest is the resistance mutation Arg-243-Met identified from dinitroaniline-resistant L. rigidum that causes helical growth when plants are homozygous for the mutation. The recessive nature of the TSR, plus possible fitness cost for some resistance mutations, likely slows resistance evolution. Furthermore, non-target-site resistance (NTSR) to dinitroanilines has been rarely reported and only confirmed in Lolium rigidum due to enhanced herbicide metabolism (metabolic resistance). A cytochrome P450 gene (CYP81A10) has been recently identified in L. rigidum that confers resistance to trifluralin. Moreover, TSR and NTSR have been shown to co-exist in the same weedy species, population, and plant. The implication of knowledge and information on TSR and NTSR in management of dinitroaniline resistance is discussed.

scholarly journals Genome-wide gene expression profiling reveals that cuticle alterations and P450 detoxification are associated with pyrethroid resistance in Anopheles arabiensis populations from Ethiopia

2018 ◽  
Author(s):  
Eba Alemayehu Simma ◽  
Wannes Dermauw ◽  
Vasileia Balabanidou ◽  
Simon Snoeck ◽  
Astrid Bryon ◽  
...  
Keyword(s):  
Insecticide Resistance ◽  
Anopheles Arabiensis ◽  
Pyrethroid Resistance ◽  
Resistance Mutation ◽  
Resistance Mechanisms ◽  
Target Site ◽  
Malaria Vectors ◽  
Metabolic Resistance ◽  
Genome Wide ◽  
Target Site Resistance

AbstractBACKGROUNDVector control is the main intervention in malaria control and elimination strategies. However, the development of insecticide resistance is one of the major challenges for controlling malaria vectors. Anopheles arabiensis populations in Ethiopia showed resistance against both DDT and the pyrethroid deltamethrin. Although a L1014F target-site resistance mutation was present in the voltage gated sodium channel of investigated populations, the levels of resistance and biochemical studies indicated the presence of additional resistance mechanisms. In this study, we used genome-wide transcriptome profiling by RNAseq to assess differentially expressed genes between three deltamethrin and DDT resistant An. arabiensis field populations (Tolay, Asendabo, Chewaka) and two susceptible strains (Sekoru and Mozambique).RESULTSBoth RNAseq analysis and RT-qPCR showed that a glutathione-S-transferase, gstd3, and a cytochrome P450 monooxygenase, cyp6p4, were significantly overexpressed in the group of resistant populations compared to the susceptible strains, suggesting that the enzymes they encode play a key role in metabolic resistance against deltamethrin or DDT. Furthermore, a gene ontology enrichment analysis showed that expression changes of cuticle related genes were strongly associated with insecticide resistance, although this did not translate in increased thickness of the procuticle.CONCLUSIONOur transcriptome sequencing of deltamethrin/DDT resistant An. arabiensis populations from Ethiopia suggests non-target site resistance mechanisms and pave the way for further investigation of the role of cuticle composition in resistance.

scholarly journals Target-Site and Non-target-Site Resistance Mechanisms Confer Multiple and Cross- Resistance to ALS and ACCase Inhibiting Herbicides in Lolium rigidum From Spain

2021 ◽  
Vol 12 ◽  
Author(s):  
Joel Torra ◽  
José María Montull ◽  
Andreu Taberner ◽  
Nawaporn Onkokesung ◽  
Neil Boonham ◽  
...  
Keyword(s):  
Glutathione Transferase ◽  
Point Mutations ◽  
Acetolactate Synthase ◽  
Target Site ◽  
Cross Resistance ◽  
Lolium Rigidum ◽  
P450 Monooxygenase ◽  
Winter Cereals ◽  
Target Site Resistance ◽  
Sites Of Action

Lolium rigidum is one the worst herbicide resistant (HR) weeds worldwide due to its proneness to evolve multiple and cross resistance to several sites of action (SoA). In winter cereals crops in Spain, resistance to acetolactate synthase (ALS)- and acetyl-CoA carboxylase (ACCase)-inhibiting herbicides has become widespread, with farmers having to rely on pre-emergence herbicides over the last two decades to maintain weed control. Recently, lack of control with very long-chain fatty acid synthesis (VLCFAS)-inhibiting herbicides has been reported in HR populations that are difficult to manage by chemical means. In this study, three Spanish populations of L. rigidum from winter cereals were confirmed as being resistant to ALS- and ACCase-inhibiting herbicides, with broad-ranging resistance toward the different chemistries tested. In addition, reduced sensitivity to photosystem II-, VLCFAS-, and phytoene desaturase-inhibiting herbicides were confirmed across the three populations. Resistance to ACCase-inhibiting herbicides was associated with point mutations in positions Trp-2027 and Asp-2078 of the enzyme conferring target site resistance (TSR), while none were detected in the ALS enzyme. Additionally, HR populations contained enhanced amounts of an ortholog of the glutathione transferase phi (F) class 1 (GSTF1) protein, a functional biomarker of non-target-site resistance (NTSR), as confirmed by enzyme-linked immunosorbent assays. Further evidence of NTSR was obtained in dose-response experiments with prosulfocarb applied post-emergence, following pre-treatment with the cytochrome P450 monooxygenase inhibitor malathion, which partially reversed resistance. This study confirms the evolution of multiple and cross resistance to ALS- and ACCase inhibiting herbicides in L. rigidum from Spain by mechanisms consistent with the presence of both TSR and NTSR. Moreover, the results suggest that NTSR, probably by means of enhanced metabolism involving more than one detoxifying enzyme family, confers cross resistance to other SoA. The study further demonstrates the urgent need to monitor and prevent the further evolution of herbicide resistance in L. rigidum in Mediterranean areas.

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 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.

ALK resistance mutations and co-occurring genetic alterations to the ALK tyrosine kinase inhibitors in lung cancer.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e20675-e20675 ◽  
Author(s):  
Jin-Ji Yang ◽  
Chi Zhang ◽  
Jun Zhao ◽  
Pingping Dai ◽  
Gen Lin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
Point Mutations ◽  
Resistance Mutation ◽  
Genetic Alterations ◽  
Driver Gene ◽  
Resistance Mutations ◽  
Significant Difference

e20675 Background: Acquired ALK mutations pose a challenge in multiple ALK tyrosine kinase inhibitors (TKIs) for lung cancer. In our study, we examined the profiles of ALK resistance mutations and co-occurring genetic alterations after targeted therapy. Methods: Using targeted gene capture and next-generation sequencing technologies, we analyzed the somatic mutations from174 patients (pts) with post-TKI samples. Among them, 123 pts received first-generation TKI crizotinib only, 51 pts (34 with second-generation TKI, 17 with third-generation TKI) treated with multiple ALK-TKIs. Results: After the treatment of ALK-TKIs, 29% (50/174) patients developed ALK resistance point mutations, including G1202R (22 pts), G1269A (13 pts), L1196M (8 pts), D1203N (5 pts), F1174L (4 pts), I1171T (4 pts), E1210K (4 pts), G1128A (3 pts), F1174C (3 pts), C1156Y (1 pts), G1123S (1 pts), I1171S (1 pts), L1152R (1 pts), and 10 of them had multi-clone. Specifically, G1269A was found a higher proportion in crizotinib group contrast to multi-TKIs cohort (10/24 vs 3/26, p = 0.024). The recalcitrant G1202R was another common resistance mutation, but there was no significant difference between the two groups (p = 0.052). Other concurrent genetic alterations related to clinical response were usually observed in TP53 mutations (46%), furthermore it seemed to be more frequently detected in post-crizotinb compared with multi-TKIs (P = 0.023). Activated bypass signaling may promote tumor progression. In non-ALK resistance point mutations samples (n = 124), co-occurring genomic alterations in EGFR (32/124, p = 0.004) were significantly more enriched in crizotinib group (n = 99). The driver gene mutation may limit crizotinib response. However, EP300 (24%), CDKN2A (12%), TRIM58 (12%), STK11 (12%) or KRAS (8%) mutations were common in the multiple ALK-TKIs group (n = 25). Conclusions: In lung cancer patients, ALK resistance point mutations G1269A was significantly enriched in post-crizotinib, while patients with multiple ALK-TKIs may frequently found G1202R or L1196M. The co-occurring genetic alterations in TP53 or EGFR after the TKIs therapeutic may offer directions for further research and therapy in lung cancer.

scholarly journals Insecticide resistance selection and reversal in two strains of Aedes aegypti

2020 ◽  
Vol 5 ◽  
pp. 183
Author(s):  
Jonathan Thornton ◽  
Bruno Gomes ◽  
Constância Ayres ◽  
Lisa Reimer
Keyword(s):  
Aedes Aegypti ◽  
Insecticide Resistance ◽  
Vector Competence ◽  
Resistance Mechanisms ◽  
Target Site ◽  
Metabolic Resistance ◽  
Resistance Selection ◽  
Similar Phenotype ◽  
Target Site Resistance ◽  
Homozygous Resistant

Background: Laboratory reared mosquito colonies are essential tools to understand insecticide action. However, they differ considerably from wild populations and from each other depending on their origin and rearing conditions, which makes studying the effects of specific resistance mechanisms difficult. This paper describes our methods for establishing multiple resistant strains of Aedes aegypti from two colonies as a new resource for further research on metabolic and target site resistance. Methods: Two resistant colonies of Ae. aegypti, from Cayman and Recife, were selected through 10 generations of exposure to insecticides including permethrin, malathion and temephos, to yield eight strains with different profiles of resistance due to either target site or metabolic resistance. Resistance ratios for each insecticide were calculated for the selected and unselected strains. The frequency of kdr alleles in the Cayman strains was determined using TaqMan assays. A comparative gene expression analysis among Recife strains was conducted using qPCR in larvae (CCae3A, CYP6N12, CYP6F3, CYP9M9) and adults (CCae3A, CYP6N12, CYP6BB2, CYP9J28a). Results: In the selected strain of Cayman, mortality against permethrin reduced almost to 0% and kdr became fixated by 5 generations. A similar phenotype was seen in the unselected homozygous resistant colony, whilst mortality in the susceptible homozygous colony rose to 82.9%. The Recife strains showed different responses between exposure to adulticide and larvicide, with detoxification genes in the temephos selected strain staying similar to the baseline, but a reduction in detoxification genes displayed in the other strains. Conclusions: These selected strains, with a range of insecticide resistance phenotypes and genotypes, will support further research on the effects of target-site and/or metabolic resistance mechanisms on various life-history traits, behaviours and vector competence of this important arbovirus vector.

scholarly journals Point Mutations and Cytochrome P450 Can Contribute to Resistance to ACCase-Inhibiting Herbicides in Three Phalaris Species

Plants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1703
Author(s):  
José G. Vázquez-García ◽  
Joel Torra ◽  
Candelario Palma-Bautista ◽  
Ricardo Alcántara-de la Cruz ◽  
Rafael De Prado
Keyword(s):  
Point Mutations ◽  
Resistance Mechanisms ◽  
Target Site ◽  
In Vitro Assays ◽  
Cross Resistance ◽  
Northern Iran ◽  
Target Site Resistance ◽  
Acetyl Coenzyme A Carboxylase ◽  
Selection Of

Species of Phalaris have historically been controlled by acetyl-coenzyme A carboxylase (ACCase)-inhibiting herbicides; however, overreliance on herbicides with this mechanism of action has resulted in the selection of resistant biotypes. The resistance to ACCase-inhibiting herbicides was characterized in Phalaris brachystachys, Phalaris minor, and Phalaris paradoxa samples collected from winter wheat fields in northern Iran. Three resistant (R) biotypes, one of each Phalaris species, presented high cross-resistance levels to diclofop-methyl, cycloxydim, and pinoxaden, which belong to the chemical families of aryloxyphenoxypropionates (FOPs), cyclohexanediones (DIMs), and phenylpyrazolines (DENs), respectively. The metabolism of 14C-diclofop-methyl contributed to the resistance of the P. brachystachys R biotype, while no evidence of herbicide metabolism was found in P. minor or P. paradoxa. ACCase in vitro assays showed that the target sites were very sensitive to FOP, DIM, and DEN herbicides in the S biotypes of the three species, while the R Phalaris spp. biotypes presented different levels of resistance to these herbicides. ACCase gene sequencing confirmed that cross-resistance in Phalaris species was conferred by specific point mutations. Resistance in the P. brachystachys R biotype was due to target site and non-target-site resistance mechanisms, while in P. minor and P. paradoxa, only an altered target site was found.

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