Negative Cross-Resistance of Acetolactate Synthase Inhibitor–Resistant Kochia (Kochia scoparia) to Protoporphyrinogen Oxidase– and Hydroxyphenylpyruvate Dioxygenase–Inhibiting Herbicides

2012 ◽  
Vol 26 (3) ◽  
pp. 570-574 ◽  
Author(s):  
Hugh J. Beckie ◽  
Eric N. Johnson ◽  
Anne Légère
Keyword(s):  
Growth And Development ◽  
Null Hypothesis ◽  
Acetolactate Synthase ◽  
Pleiotropic Effect ◽  
Cross Resistance ◽  
Kochia Scoparia ◽  
Protoporphyrinogen Oxidase ◽  
Synthase Inhibitor ◽  
Sites Of Action ◽  
Als Inhibitor

This greenhouse experiment examined the response of homozygous susceptible and acetolactate synthase (ALS) inhibitor–resistant plants from six Canadian kochia accessions with the Pro197 or Trp574 mutation to six alternative herbicides of different sites of action. The null hypothesis was ALS-inhibitor–resistant and –susceptible plants from within and across accessions would respond similarly to herbicides of different sites of action. This hypothesis was accepted for all accessions except that of MBK2 with the Trp574 mutation. Resistant plants of that accession were 80, 60, and 50% more sensitive than susceptible plants to pyrasulfotole, mesotrione (hydroxyphenylpyruvate dioxygenase [HPPD] inhibitors), and carfentrazone (protoporphyrinogen oxidase [PPO] inhibitor), respectively. However, no differential dose response between resistant and susceptible plants of this kochia accession to bromoxynil, fluroxypyr, or glyphosate was observed. A previous study had found marked differences in growth and development between resistant and susceptible plants of this accession, but not of the other accessions examined in this experiment. Negative cross-resistance exhibited by resistant plants of accession MBK2 to PPO and HPPD inhibitors in this experiment may be a pleiotropic effect related to the Trp574 mutation.

scholarly journals Nontarget site resistance in Palmer amaranth [Amaranthus palmeri(S.) Wats.] confers cross-resistance to protoporphyrinogen oxidase-inhibiting herbicides

2019 ◽  
Vol 33 (2) ◽  
pp. 349-354 ◽  
Author(s):  
Vijay K. Varanasi ◽  
Chad Brabham ◽  
Nicholas E. Korres ◽  
Jason K. Norsworthy
Keyword(s):  
Resistance Index ◽  
Acetolactate Synthase ◽  
Palmer Amaranth ◽  
Cross Resistance ◽  
Multiple Resistance ◽  
Protoporphyrinogen Oxidase ◽  
First Case ◽  
Sites Of Action ◽  
Als Inhibitor ◽  
Biomass Reduction

AbstractPalmer amaranth is one of the most problematic weeds in cropping systems of North America, especially in midsouthern United States, because of its competitive ability and propensity to evolve resistance to several herbicide sites of action. Previously, we confirmed and characterized the first case of nontarget site resistance (NTSR) to fomesafen in a Palmer amaranth accession from Randolph County, AR (RCA). The primary basis of the present study was to evaluate the cross- and multiple-resistance profile of the RCA accession. The fomesafen dose-response assay in the presence of malathion revealed a lower level of RCA resistance when compared with fomesafen alone. The resistance index of the RCA accession, based on 50% biomass reduction, ranged from 63-fold (fomesafen alone) to 22-fold (malathion plus fomesafen), when compared with a 2007 susceptible, and 476-fold and 167-fold, respectively, relative to a 1986 susceptible check. The RCA accession was resistant to other protoporphyrinogen oxidase (PPO) inhibitors (i.e., flumioxazin, acifluorfen, saflufenacil) as well as the 4-hydroxyphenylpyruvate dioxygenase (HPPD) inhibitor tembotrione and acetolactate synthase (ALS) inhibitor pyrithiobac sodium. Sequencing of theALSgene revealed no point mutations, indicating that a target-site mechanism is not involved in conferring ALS-inhibitor resistance in the RCA accession. Of the three PPO-inhibiting herbicides tested in combination with the malathion, saflufenacil resulted in the greatest biomass reduction (80%;P< 0.05) and lowest survival rate (23%;P< 0.05) relative to nontreated plants. The application of cytochrome P450 or glutathioneS-transferase inhibitors with fomesafen did not lead to any adverse effects on soybean, suggesting a possible role for these compounds for management of NTSR under field conditions. These results shed light on the relative unpredictability of NTSR in conferring herbicide cross- and multiple resistance in Palmer amaranth.

scholarly journals Biology, management and biochemical/genetic characterization of weed biotypes resistant to acetolactate synthase inhibitor herbicides

2003 ◽  
Vol 60 (3) ◽  
pp. 495-503 ◽  
Author(s):  
Patrícia Andrea Monquero ◽  
Pedro Jacob Christoffoleti ◽  
Helaine Carrer
Keyword(s):  
Research Work ◽  
Acetolactate Synthase ◽  
Pleiotropic Effect ◽  
Cross Resistance ◽  
Bidens Pilosa ◽  
Glycine Max L ◽  
Biochemical Genetic ◽  
Synthase Inhibitor ◽  
Imidazolinone Herbicides ◽  
Als Inhibitor

Bidens pilosa and Amaranthus quitensis are major weeds infesting soybean [Glycine max L (Merrill)] fields in Brazil and Argentina. The repetitive use of acetolactate synthase (ALS EC 4.1.3.18) inhibiting herbicides in São Gabriel do Oeste, MS, Brazil and in the provinces of Córdoba and Tucumã, Argentina, has selected for resistant (R) biotypes of these weeds. Research work was developed to study the management, growth, biochemistry, and genetics of these R weed biotypes. In a field experiment it was found that chlorimuron-ethyl and imazethapyr at recommended rates (both ALS inhibitor herbicides), did not control R B. pilosa, but the alternative lactofen, fomesafen and bentazon were effective, either sprayed alone or mixed with the ALS inhibitor herbicides. Greenhouse studies confirmed the cross-resistance of both R biotypes to the imidazolinone and sulfonylurea herbicides, and these alternative herbicides, when sprayed alone or mixed with the ALS inhibitor, efficiently controlled both R and S populations. A growth analysis of the R and S biotypes of these weeds, under non-competitive conditions, indicated that there is no adaptive cost to the R biotypes (pleiotropic effect). A quick bioassay using ALS and ketoacid reductoisomerase (KARI) inhibitors showed that the resistance of the R biotypes to herbicides is related to a lack of sensitivity of the ALS enzyme to the herbicides. On the other hand, the sequencing of the gene that codifies the ALS resistance in R A. quitensis did not present any mutation in the A Domain region, suggesting that other positions of the gene that confer insensitivity of the ALS to sulfonylurea and imidazolinone herbicides could have mutated.

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

Glyphosate- and acetolactate synthase inhibitor-resistant kochia (Bassia scoparia) control in field pea

2021 ◽  
Author(s):  
Alysha T Torbiak ◽  
Robert Blackshaw ◽  
Randall N Brandt ◽  
Bill Hamman ◽  
Charles M. Geddes
Keyword(s):  
Great Plains ◽  
Field Experiments ◽  
Rapid Evolution ◽  
Acetolactate Synthase ◽  
Field Pea ◽  
Visible Injury ◽  
Crop Harvest ◽  
Selection For ◽  
Synthase Inhibitor ◽  
Als Inhibitor

Kochia [Bassia scoparia (L.) A.J. Scott] is an invasive C4 tumbleweed in the Great Plains of North America, where it impedes crop harvest and causes significant crop yield losses. Rapid evolution and spread of glyphosate- and acetolactate synthase (ALS) inhibitor-resistant kochia in western Canada limit the herbicide options available for control of these biotypes in field pea (Pisum sativum L.); one of the predominant pulse crops grown in this region. Field experiments were conducted near Lethbridge, Alberta in 2013-2015 and Coalhurst, Alberta in 2013-2014 to determine which herbicide options effectively control glyphosate- and ALS inhibitor-resistant kochia in field pea. Visible injury of field pea was minor (0-4%) in all environments except for Lethbridge 2013, where pre-plant (PP) flumioxazin and all treatments containing post-emergence (POST) imazamox/bentazon resulted in unacceptable (14-23%) pea visible injury. Herbicide impacts on pea yield were minor overall. Carfentrazone + sulfentrazone PP and saflufenacil PP followed by imazamox/bentazon POST resulted in ≥80% visible control of kochia in all environments, while POST imazamox/bentazon alone resulted in ≥80% reduction in kochia biomass in all environments compared with the untreated control (albeit absent of statistical difference in Coalhurst 2014). These results suggest that layering the protoporhyrinogen oxidase-inhibiting herbicides saflufenacil or carfentrazone + sulfentrazone PP with the ALS- and photosystem II-inhibiting herbicide combination imazamox/bentazon POST can effectively control glyphosate- and ALS inhibitor-resistant kochia in field pea while also mitigating further selection for herbicide resistance through the use of multiple effective herbicide modes-of-action.

In vitro and whole-plant magnitude and cross-resistance characterization of two imidazolinone-resistant sugarbeet (Beta vulgaris) somatic cell selections

Weed Science ◽  
1998 ◽  
Vol 46 (1) ◽  
pp. 24-29 ◽  
Author(s):  
Terry R. Wright ◽  
Donald Penner
Keyword(s):  
Somatic Cell ◽  
Shoot Culture ◽  
Acetolactate Synthase ◽  
Cross Resistance ◽  
Shoot Cultures ◽  
Als Inhibitors ◽  
Whole Plants ◽  
Inhibitor Resistance ◽  
Als Inhibitor

Acetolactate synthase (ALS)-inhibiting herbicide carryover in soil can severely affect sugarbeets grown in the year(s) following application. Two newly developed imidazolinone-resistant (IMI-R) sugarbeet somatic cell selections (Sir-13 and 93R30B) were examined for magnitude of resistance and extent of cross-resistance to other classes of ALS inhibitors and compared to a previously developed sulfonylurea-resistant (SU-R) selection, Sur. In vitro shoot culture tests indicated Sir-13 resistance was specific to imidazolinone (IMI) herbicides at approximately a 100-fold resistance compared to the sensitive control sugarbeet. Sur was 10,000-fold resistant to the sulfonylurea (SU) herbicide, chlorsulfuron, and 40-fold resistant to the triazolopyrimidine sulfonanilide (TP) herbicide, flumetsulam, but not cross-resistant to the IMI herbicides. 93R30B was selected for IMI-R from a plant homozygous for the SU-R allele,Sur, and displayed similar in vitro SU-R and TP-R as Sur, but also displayed a very high resistance to various IMI herbicides (400- to 3,600-fold). Compared to the sensitive control, Sir-13 was 300- and > 250-fold more resistant to imazethapyr and imazamox residues in soil, respectively. Response by whole plants to postemergence herbicide applications was similar to that observed in shoot cultures. Sir-13 exhibited > 100-fold resistance to imazethapyr as well as imazamox, and 93R30B showed > 250-fold resistance to both herbicides. 93R30B showed great enough resistance to imazamox to merit consideration of imazamox for use as a herbicide in these sugarbeets. Sir-13 showed a two- to threefold higher level of resistance in the homozygous vs. heterozygous state, indicating that like most ALS-inhibitor resistance traits, it was semidominantly inherited.

Acetolactate Synthase Inhibitor–Resistant False Cleavers (Galium spurium) in Western Canada

2012 ◽  
Vol 26 (1) ◽  
pp. 151-155 ◽  
Author(s):  
Hugh J. Beckie ◽  
Suzanne I. Warwick ◽  
Connie A. Sauder ◽  
Gina M. Kelln ◽  
Chris Lozinski
Keyword(s):  
Point Mutations ◽  
Low Frequency ◽  
Acetolactate Synthase ◽  
Western Canada ◽  
Resistance Factors ◽  
Als Inhibitors ◽  
Synthase Inhibitor ◽  
Inhibitor Resistance ◽  
Als Inhibitor ◽  
Galium Spurium

Cleavers species (false cleavers and catchweed bedstraw) are among the top 10 most abundant weeds across the prairie region of western Canada, and are increasing in relative abundance at the fastest rate since the 1970s. In 2008, two false cleavers populations from Tisdale and Choiceland, Saskatchewan, were suspected of acetolactate synthase (ALS) –inhibitor resistance. Dose-response experiments were conducted with the use of imazethapyr and florasulam, both ALS inhibitors, as well as fluroxypyr, a synthetic auxin. Additionally, a 1,954–base-pair region of theALSgene including sites known to conferALSresistance were sequenced. Both populations were highly resistant to imazethapyr (resistance factors greater than 100), one population (Tisdale) was highly resistant to florasulam (Choiceland population susceptible, although a second, larger screening of 200 individuals indicated low frequency [2%] florasulam resistance), and both populations were susceptible to fluroxypyr. All sequenced Tisdale individuals screened with imazethapyr posessed the Trp574Leu mutation. In contrast, three point mutations were found for Choiceland individuals sequenced: Ser653Asn, Trp574Leu, and Asp376Glu. TheseALStarget-site mutations have not been documented previously in this species.

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.

scholarly journals Evaluation of Preemergence Herbicide Programs for Control of Protoporphyrinogen Oxidase-Resistant Amaranthus palmeri in Soybean

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Michael M. Houston ◽  
L. Tom Barber ◽  
Jason K. Norsworthy ◽  
Trent L. Roberts
Keyword(s):  
Acetolactate Synthase ◽  
Field Trials ◽  
Palmer Amaranth ◽  
Amaranthus Palmeri ◽  
Long Chain Fatty Acid ◽  
Protoporphyrinogen Oxidase ◽  
Density Reduction ◽  
Glycine Max L ◽  
Sites Of Action ◽  
Herbicide Programs

Protoporphyrinogen oxidase- (PPO-) resistant Amaranthus palmeri (S.) Wats. (Palmer amaranth) was confirmed in Arkansas in 2015. Field trials were conducted in Crawfordsville, Gregory, and Marion, Arkansas in 2016, and Crawfordsville and Marion in 2017, assessing PPO-resistant Palmer amaranth control options in Glycine max (L.) Merr. (soybean). Twelve trials consisted of 26 preemergence (PRE) treatments, evaluated for Palmer amaranth control and density reduction at 28 days after treatment (DAT). Treatments that consisted of PPO- or acetolactate synthase- (ALS-) inhibiting herbicides such as flumioxazin (72 g ai ha−1) or sulfentrazone + cloransulam (195 g ha−1 + 25 g ha−1) controlled Palmer amaranth <60%. At 28 DAT, treatments including mixtures of a very-long-chain fatty acid (VLCFA) plus the photosystem II- (PSII-) inhibiting herbicide metribuzin provided increased control over single herbicide sites of action (SOA) or herbicides mixtures to which Palmer amaranth was resistant. Pyroxasulfone + metribuzin (149 g ha−1 + 314 g ha−1) controlled Palmer amaranth 91% control across twelve trials at 28 DAT. S-metolachlor alone did not provide consistent, acceptable control of PPO-resistant Palmer amaranth (55–77%); subsequent research has determined that these populations are resistant to S-metolachlor. A minimum of two effective herbicides should be included in soybean PRE programs for control of PPO-resistant Palmer amaranth.

scholarly journals The occurrence of herbicide-resistant Avena fatua (wild oats) populations to ACCase-inhibiting herbicides in Ireland

2021 ◽  
Author(s):  
R. Byrne ◽  
A.V. Vijaya Bhaskar ◽  
J. Spink ◽  
R. Freckleton ◽  
P. Neve ◽  
...  
Keyword(s):  
Herbicide Resistance ◽  
Weed Management ◽  
Resistance Mechanism ◽  
Point Mutations ◽  
Acetolactate Synthase ◽  
Avena Fatua ◽  
Integrated Weed Management ◽  
Cross Resistance ◽  
Wild Oats ◽  
Als Inhibitor

Following growers’ reports of herbicide control problems, populations of 30 wild oats, Avena fatua, were collected from the south-east main arable counties of Ireland in 2016 and investigated for the occurrence and potential for herbicide resistance to acetyl-CoA carboxylase (ACCase) inhibitors pinoxaden, propaquizafop and cycloxydim, as well as acetolactate synthase (ALS) inhibitor mesosulfuron + iodosulfuron. Plant survival ≥20% was considered as the discriminating threshold between resistant and susceptible populations, when plants were treated with full recommended field rates of ACCase/ALS inhibitors. Glasshouse sensitivity screens revealed 2 out of 30 populations were cross-resistant to all three ACCase inhibitors. While three populations were cross-resistant to both pinoxaden and propaquizafop, and additionally, two populations were resistant to propaquizafop only. Different degree of resistance and cross-resistance between resistant populations suggest the involvement of either different point mutations or more than one resistance mechanism. Nevertheless, all populations including the seven ACCase-resistant populations were equally susceptible to ALS inhibitor. An integrated weed management (cultural/non-chemical control tactics and judicious use of herbicides) approach is strongly recommended to minimize the risk of herbicide resistance evolution.

Comparison of ALS inhibitor resistance and allelic interactions in shattercane accessions

Weed Science ◽  
1999 ◽  
Vol 47 (3) ◽  
pp. 275-281 ◽  
Author(s):  
Chad D. Lee ◽  
Alex R. Martin ◽  
Fred W. Roeth ◽  
Blaine E. Johnson ◽  
Donald J. Lee
Keyword(s):  
Sorghum Bicolor ◽  
Acetolactate Synthase ◽  
Cross Resistance ◽  
Wild Type ◽  
Forage Sorghum ◽  
South Central ◽  
Inhibitor Resistance ◽  
Als Inhibitor

Reports of unacceptable shattercane (Sorghum bicolor) control with acetolactate synthase (ALS)-inhibiting herbicides prompted the investigation of 29 fields in central and south-central Nebraska for ALS-resistant (ALSr) shattercane. These fields were located in three distinct geographical areas designated C, G, and P. Shattercane from 13 fields spanning all three areas was resistant to 80 g ai ha−1(2 X field rate) primisulfuron. Accessions C and G were more resistant than accession P to primisulfuron and nicosulfuron. Accessions C and G were susceptible to imazethapyr, whereas accession P was resistant. The ALS resistance was associated with alterations in the ALS enzyme. Primisulfuron I50values for ALS from ROX (forage sorghum), C, G, and P were 7, 8,510, 8,870, and 714 nM, respectively; nicosulfuron I50values were 647, 4,110, 4,070, and 1,460 nM, respectively; and imazethapyr I50values were 5,440, 13,100, 11,800, and 51,700 nM, respectively. Based on cross-resistance and enzyme sensitivities, at least two biotypes are represented in the three accessions of ALSr shattercane. Shattercane individuals from accessions C, G, and P were intercrossed to determine if the ALSr genes in each of the accessions were at independent loci. All the F2populations were resistant to 80 g ai ha−1primisulfuron, suggesting that the ALSr alleles in the three accessions are at the same locus or possibly linked loci. When the C, G, and P accessions were crossed with the wild type (WT), comparisons between the F1, susceptible, and resistant populations showed that primisulfuron resistance was expressed as a dominant, partially dominant, and additive trait for the C, G, and P accessions, respectively. The differences in ALSr allelic interactions indicate that primisulfuron resistance developed independently in each of the three accessions.

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