The target-site based resistance mechanism of Alopecurus myosuroides Huds. to pyroxsulam

2021 ◽  
pp. 105707
Author(s):  
Zhaofeng Huang ◽  
Xingtao Lu ◽  
Shouhui Wei ◽  
Chaoxian Zhang ◽  
Cuilan Jiang ◽  
...  
Keyword(s):  
Resistance Mechanism ◽  
Target Site ◽  
Alopecurus Myosuroides

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.

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 Comparison of the knockdown resistance locus (kdr) in Anopheles stephensi, An. arabiensis, and Culex pipiens s.l. suggests differing mechanisms of pyrethroid resistance in east Ethiopia

2020 ◽  
Author(s):  
Tamar E. Carter ◽  
Araya Gebresilassie ◽  
Shantoy Hansel ◽  
Lambodhar Damodaran ◽  
Callum Montgomery ◽  
...  
Keyword(s):  
Insecticide Resistance ◽  
Culex Pipiens ◽  
Anopheles Stephensi ◽  
Pyrethroid Resistance ◽  
Resistance Mechanism ◽  
Target Site ◽  
Resistance Locus ◽  
Knockdown Resistance ◽  
Resistance Mutations ◽  
Vector Species

AbstractThe malaria vector, Anopheles stephensi, which is typically restricted to South Asia and the Middle East, was recently detected in the Horn of Africa. Controlling the spread of this vector could involve integrated vector control that considers the status of insecticide resistance of multiple vector species in the region. Previous reports indicate that the knockdown resistance mutations (kdr) in the voltage-gated sodium channel (vgsc) are absent in both pyrethroid resistant and sensitive variants of An. stephensi in east Ethiopia but similar information on other vector species in the same areas is limited. In this study, kdr and the neighboring intron was analyzed in An. stephensi, An. arabiensis, and Culex pipiens s. l. collected in east Ethiopia between 2016 and 2017. Sequence analysis revealed that all of Cx. pipiens s.l. (n = 42) and 71.6% of the An. arabiensis (n=67) carried kdr L1014F known to confer target-site pyrethroid resistance. Intronic variation was only observed in An. stephensi (segregating sites = 6, haplotypes = 3) previously shown to have no kdr mutations. In addition, no evidence of non-neutral evolutionary processes was detected at the An. stephensi kdr intron which further supports target-site mechanism not being a major resistance mechanism in this An. stephensi population. Overall, these results suggest differences in evolved mechanisms of pyrethroid/DDT resistance in populations of vector species from the same region. Variation in insecticide resistance mechanisms in East Ethiopian mosquito vectors highlight possible species or population specific biological factors and distinct environmental exposures that shape their evolution.

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.

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.

scholarly journals Investigating target‐site resistance mechanism to the PPO‐inhibiting herbicide fomesafen in waterhemp and interspecific hybridization of Amaranthus species using next generation sequencing

2019 ◽  
Vol 75 (12) ◽  
pp. 3235-3244 ◽  
Author(s):  
Haozhen Nie ◽  
Brent C Mansfield ◽  
Nick T Harre ◽  
Julie M Young ◽  
Nicholas R Steppig ◽  
...  
Keyword(s):  
Next Generation Sequencing ◽  
Interspecific Hybridization ◽  
Resistance Mechanism ◽  
Target Site ◽  
Next Generation ◽  
Target Site Resistance ◽  
Generation Sequencing
Sign in / Sign up

Export Citation Format

Share Document