Cross-resistance patterns to ACCase-inhibiting herbicides conferred by mutant ACCase isoforms in Alopecurus myosuroides Huds. (black-grass), re-examined at the recommended herbicide field rate

BACKGROUND: Target‐site‐based resistance to acetyl‐CoA carboxylase (ACCase) inhibitors in Alopecurus myosuroides Huds. is essentially due to five substitutions (Isoleucine‐1781‐Leucine, Tryptophan‐2027‐Cysteine, Isoleucine‐2041‐Asparagine, Aspartate‐2078‐Glycine, Glycine‐2096‐Alanine). Recent studies suggested that cross‐resistance patterns associated with each mutation using a seed‐based bioassay may not accurately reflect field resistance. The authors aimed to connect the presence of mutant ACCase isoform(s) in A. myosuroides with resistance to five ACCase inhibitors (fenoxaprop, clodinafop, haloxyfop, cycloxydim, clethodim) sprayed at the recommended field rate. RESULTS: Results from spraying experiments and from seed‐based bioassays were consistent for all mutant isoforms except the most widespread, Leucine‐1781. In spraying experiments, Leucine‐1781 ACCase conferred resistance to clodinafop and haloxyfop. Some plants containing Leucine‐1781 or Alanine‐2096 ACCase, but not all, were also resistant to clethodim. CONCLUSION: Leucine‐1781, Cysteine‐2027, Asparagine‐2041 and Alanine‐2096 ACCases confer resistance to fenoxaprop, clodinafop and haloxyfop at field rates. Leucine‐1781 ACCase also confers resistance to cycloxydim at field rate. Glycine‐2078 ACCase confers resistance to all five herbicides at field rates. Only Glycine‐2078 ACCase confers clethodim resistance under optimal application conditions. It may be that Leucine‐1781 and Alanine‐2096 ACCases may also confer resistance to clethodim in the field if the conditions are not optimal for herbicide efficacy, or at reduced clethodim field rates. Copyright © 2008 Society of Chemical Industry     

Cross‐resistance patterns to acetyl coenzyme A carboxylase (ACCase) inhibitors associated with different ACCase mutations in Beckmannia syzigachne

Beckmannia syzigachne (American sloughgrass) is a competitive grass weed found in China. Fenoxaprop‐P‐ethyl is widely used for control of this species in China. Resistance to fenoxaprop‐P‐ethyl in B. syzigachne has been reported to be conferred by an isoleucine(Ile)‐1781‐leucine(Leu) substitution in the gene encoding the herbicide target, acetyl‐CoA carboxylase (ACCase). In this study, three mutations were detected by derived cleaved amplified polymorphic sequence (dCAPS) method in fenoxaprop‐P‐ethyl‐resistant B. syzigachne populations: Ile‐1781‐Leu in population JCWL‐R, Ile‐2041‐Asn in JCJT‐R and Gly‐2096‐Ala in JYJD‐R. The data indicated they were genetically homogeneous (homozygous mutant) at the ACCase locus. The use of cytochrome P450 inhibitors was shown to slightly reduce the GR₅₀ value of fenoxaprop‐P‐ethyl‐resistant populations, from which we inferred a combination of target‐site resistance (TSR) and non‐target‐site resistance (NTSR) was involved in fenoxaprop‐P‐ethyl‐resistance. We characterised the cross‐resistance patterns to ACCase inhibitors in B. syzigachne. The plants in the JCWL‐R population were highly resistant to all tested APPs (aryloxyphen‐oxypropionates), sethoxydim and pinoxaden, and moderately resistant to clethodim. The plants in the JCJT‐R population were highly resistant to fluazifop‐P‐butyl, clodinafop‐propargyl, cyhalofop‐butyl, metamifop and pinoxaden; moderately resistant to haloxyfop‐R‐methyl, quizalofop‐P‐ethyl and sethoxydim; and sensitive to clethodim. The plants in the JYJD‐R population were highly resistant to clodinafop‐propargyl, metamifop and pinoxaden; moderately resistant to haloxyfop‐R‐methyl, cyhalofop‐butyl, quizalofop‐P‐ethyl, fluazifop‐P‐butyl and sethoxydim; and sensitive to clethodim. If resistance to ACCase inhibitors is present in B. syzigachne populations in the field, then our results indicate that clethodim should be used. While we demonstrated the cross‐resistance patterns of TSR resulting from three mutations in B. syzigachne, we also demonstrated that NTSR plays a role in resistance, which will complicate weed management.     

Prevalence of cross‐ or multiple resistance to the acetyl‐coenzyme A carboxylase inhibitors fenoxaprop,clodinafop and pinoxaden in black‐grass (Alopecurus myosuroides Huds.) in France

BACKGROUND: Repeated use of acetyl‐CoA carboxylase (ACCase) inhibitors, especially fenoxaprop and clodinafop, since the late 1980s has selected for resistance in Alopecurus myosuroides Huds. (black‐grass) in France. We investigated whether resistance to pinoxaden, a phenylpyrazoline ACCase inhibitor to be marketed in France, was present in French black‐grass populations. We investigated pinoxaden resistance conferred by five mutant ACCase isoforms. Using 84 French black‐grass field samples, we also compared the frequencies of other mechanisms endowing resistance to fenoxaprop, clodinafop or pinoxaden. RESULTS: ACCase mutant isoforms Leu‐1781, Gly‐2078 and, likely, Cys‐2027 conferred cross‐resistance to pinoxaden, while isoform Asn‐2041 possibly conferred moderate resistance. Other mechanisms of resistance to fenoxaprop, clodinafop and pinoxaden were detected in 99, 68 and 64% of the samples investigated, respectively. Cross‐ or multiple resistance to fenoxaprop or clodinafop and pinoxaden was not systematically observed, suggesting a diversity of mechanisms exist. CONCLUSION: Pinoxaden resistance was observed before pinoxaden release in France. Only a fraction of the mechanisms endowing fenoxaprop or clodinafop resistance also confer pinoxaden resistance. Pinoxaden resistance was likely mostly selected for by ACCase inhibitors, and, in some cases, possibly by herbicides with other modes of action. This illustrates the necessity to use metabolisable herbicides cautiously where black‐grass has evolved non‐target‐site‐based resistance. Copyright © 2009 Society of Chemical Industry     

Molecular bases for resistance to acetyl-coenzyme A carboxylase inhibitor in Japanese foxtail (Alopecurus japonicus)

BACKGROUND: Haloxyfop‐R‐methyl is a widely used herbicide to control Poaceae weeds. Alopecurus japonicus, a widespread annual grass, can no longer be controlled by haloxyfop‐R‐methyl after continuous use of this herbicide for several years. RESULTS: Dose‐response experiments have established that the Js‐R biotype of A. japonicas has evolved resistance to aryloxyphenoxypropionates (APPs). Target‐site enzyme sensitivity experiments have established that the haloxyfop (free acid) rate causing 50% inhibition of acetyl‐CoA carboxylase (ACCase) activity (I₅₀) for the resistant (Js‐R) biotype is 11 times higher than that for the susceptible (Js‐S) biotype. In many cases, resistance to ACCase‐inhibiting herbicides is due to a resistant ACCase enzyme. Full‐length DNA and mRNA sequences of the plastidic ACCase gene were amplified. Eight single‐nucleotide differences were detected in this region. Four of the nucleotide changes were silent mutations. However, the other four nucleotide mutations caused four amino acid substitutions, replacing Arg‐1734 with Gly, Met‐1738 with Leu, Thr‐1739 with Ser and Ile‐2041 with Asn in the R biotype respectively; the substitution at position 2041 had been reported, while the other three had not. CONCLUSION: The ACCase in the Js‐R biotype was less susceptible to haloxyfop‐R‐methyl than that in the Js‐S biotype. Moreover, the amino acid substitution of Ile‐2041 with Asn might confer resistance to haloxyfop‐R‐methyl in A. japonicas. Copyright © 2012 Society of Chemical Industry     

Multiple origins for black-grass (Alopecurus myosuroides Huds) target-site-based resistance to herbicides inhibiting acetyl-CoA carboxylase

We have investigated the process of evolution of target-site-based resistance to herbicides inhibiting acetyl-CoA carboxylase (ACCase) in nine French populations of black-grass (Alopecurus myosuroides Huds). To date, two different ACCase resistant alleles are known. One contains an isoleucine-to-leucine substitution at position 1781, the second contains an isoleucine-to-asparagine substitution at position 2041. Using phylogenetic analysis of ACCase sequences, we showed that 1781Leu ACCase alleles evolved from four independent origins in the nine black-grass populations studied, while 2041Asn ACCase alleles evolved from six independent origins. No geographical structure of black-grass populations was revealed. This implies that these populations, although geographically distant, are, or have until recently been, connected by gene flows. Comparison of biological data obtained from herbicide sensitivity bioassay and molecular data showed that distinct resistance mechanisms often exist in a single black-grass population. Accumulation of different resistance mechanisms in a single plant was also demonstrated. We conclude that large-scale evolution of resistance to herbicides in black-grass is a complex phenomenon, resulting from the independent selection of various resistance mechanisms in local black-grass populations undergoing contrasted herbicide and agronomical selection pressures, and connected by gene flows whose parameters remain to be determined.     

耿氏硬草对乙酰辅酶A羧化酶类除草剂抗性水平及分子机制初探

为明确耿氏硬草Pseudosclerochloa kengiana(Ohwi)Tzvel潜在抗性种群对不同乙酰辅酶A羧化酶(ACCase)类除草剂的抗性水平及其靶标抗性的分子机制,采用剂量-反应曲线法测定了耿氏硬草对精鰁唑禾草灵、炔草酯、烯禾啶、烯草酮和唑啉草酯5种ACCase类除草剂的抗性水平,扩增并比对了耿氏硬草抗性和敏感种群间ACCase基因的差异。结果显示:与敏感种群SD-6相比,耿氏硬草种群SD-32对精鰁唑禾草灵、炔草酯、烯禾啶、烯草酮和唑啉草酯产生了不同水平的抗性,抗性倍数分别为16.5、7.5、15.0、4.4和5.7;SD-32种群ACCase基因CT区域的2078位氨基酸基因由GAT突变为GGT,导致天冬氨酸(Asp)被甘氨酸(Gly)取代。分析表明,ACCase基因2078位氨基酸的突变可能是导致耿氏硬草对ACCase类除草剂产生抗性的重要原因之一。     

First report of target-site resistance to ACCase-inhibiting herbicides in Bromus tectorum L.

Background

The prevalent and repeated use of acetyl-coenzyme A carboxylase (ACCase)-inhibiting herbicides for Bromus tectorum L. control in fine fescue (Festuca L. spp) grown for seed has selected ACCase-resistant B. tectorum populations. The objectives of this study were to (1) evaluate the response of nine B. tectorum populations to the ACCase inhibitors clethodim, sethoxydim, fluazifop-P-butyl, and quizalofop-P-ethyl and the acetolactate synthase (ALS) inhibitor sulfosulfuron and (2) characterize the resistance mechanisms.

Results

Bromus tectorum populations were confirmed to be resistant to the ACCase-inhibiting herbicides tested. The levels of resistance varied among the populations for clethodim (resistance ratio, RR = 5.1–14.5), sethoxydim (RR = 18.7–44.7), fluazifop-P-butyl (RR = 3.1–40.3), and quizalofop-P-ethyl (RR = 14.5–36). Molecular investigations revealed that the mutations Ile2041Thr and Gly2096Ala were the molecular basis of resistance to the ACCase-inhibiting herbicides. The Gly2096Ala mutation resulted in cross-resistance to the aryloxyphenoxypropionate (APP) herbicides fluazifop-P-butyl and quizalofop-P-ethyl, and the cyclohexanedione (CHD) herbicides clethodim, and sethoxydim, whereas Ile2041Thr mutation resulted in resistance only to the two APP herbicides. All B. tectorum populations were susceptible to sulfosulfuron (RR = 0.3–1.7).

Conclusions

This is the first report of target-site mutations conferring resistance to ACCase-inhibiting herbicides in B. tectorum. The results of this study suggest multiple evolutionary origins of resistance and contribute to understanding the patterns of cross-resistance to ACCase inhibitors associated with different mutations in B. tectorum. © 2023 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.     

Mechanism of resistance to fenoxaprop in Japanese foxtail (Alopecurus japonicus) from China

Japanese foxtail is one of the most common and troublesome weeds infesting cereal and oilseed rape fields in China. Repeated use during the last three decades of the ACCase-inhibiting herbicide fenoxaprop-P-ethyl to control this weed has resulted in the occurrence of resistance. Dose–response tests established that a population (AHFD-1) from eastern China had evolved high-level resistance to fenoxaprop-P-ethyl. Based on the resistance index, this resistant population of A. japonicus is 60.31-fold resistant to fenoxaprop-P-ethyl. Subsequently, only a tryptophan to cysteine substitution was identified to confer resistance to fenoxaprop-P-ethyl in this resistant population. ACCase activity tests further confirmed this substitution was linked to resistance. This is the first report of the occurrence of Trp-2027-Cys substitution of ACCase in A. japonicus. From whole-plant pot dose–response tests, we confirmed that this population conferred resistance to other APP herbicides, including clodinafop-propargyl, fluazifop-P-butyl, quizalofop-P-ethyl, haloxyfop-R-methyl, cyhalofop-butyl, metamifop, DEN herbicide pinoxaden, but not to CHD herbicides clethodim, sethoxydim. There was also no resistance observed to ALS-inhibiting herbicides sulfosulfuron, mesosulfuron-methyl, flucarbazone-sodium, pyroxsulam, Triazine herbicide prometryne and glyphosate. However, this resistant population was likely to confer slightly (or no) resistant to Urea herbicides chlortoluron and isoproturon.     

Derived cleaved amplified polymorphic sequence, a simple method to detect a key point mutation conferring acetyl CoA carboxylase inhibitor herbicide resistance in grass weeds

Substitution of isoleucine by leucine at the equivalent of residue 1781 of acetyl CoA carboxylase (ACCase) in Alopecurus myosuroides (I1781L) has been shown to be a key point mutation conferring resistance to most aryloxypropionate and cyclohexanedione herbicides in Lolium spp., A. myosuroides, Avena fatua and Setaria viridis. This substitution results from changing an adenine residue to either thymine or cytosine at position 5341 in the ACCase coding sequence of A. myosuroides and at the homologous position in the other species. The I1781L mutation can be detected by allele‐specific amplification assays. These are, however, very dependent on the conservation of the nucleotide sequences flanking the causative single nucleotide polymorphism. Moreover, such assays cannot distinguish between homozygous and heterozygous individuals in a single polymerase chain reaction reaction. Here we present an alternative derived Cleaved Amplified Polymorphic Sequence (dCAPS) method to define I1781L status in the ACCase enzyme of four grass weeds. This dCAPS approach is simple, economical, highly transferable between species and can readily distinguish homozygous Leu/Leu 1781 and heterozygous Ile/Leu 1781 resistant individuals, providing the basis for accurate measures of the frequency of the dominant Leu allele in a given population.     

Mechanisms of resistance to acetyl‐coenzyme A carboxylase‐inhibiting herbicides in a Hordeum leporinum population

A failure of acetyl‐coenzyme A carboxylase (ACCase)‐inhibiting herbicides to control a population of Hordeum leporinum Link (barleygrass) occurred following eight applications of these herbicides in both crops and pastures. This population was 7.6‐fold resistant to fluazifop‐P‐butyl compared with standard susceptible populations. The population was between 3.6‐ and 3.8‐fold resistant to other ACCase‐inhibiting herbicides, except butroxydim to which it was susceptible. ACCase extracted from resistant plants and assayed in the presence of herbicides in vitro was susceptible to fluazifop acid and other aryloxyphenoxypropanoate herbicides, but was 4‐fold less sensitive to sethoxydim compared with ACCase from susceptible plants. Resistant plants metabolised fluazifop acid about 1.3‐fold more rapidly compared with susceptible plants; however, sethoxydim was metabolised equally in both populations. Resistance to fluazifop‐P‐butyl and other aryloxyphenoxypropanoate herbicides may be the result of increased herbicide detoxification, whereas resistance to sethoxydim appears to be due to a modified target enzyme. Herbicide resistance in this population is unusual in that different mechanisms appear to confer resistance to the aryloxyphenoxypropanoate and cyclohexanedione herbicides. © 2000 Society of Chemical Industry     

Multiple herbicide resistance in littleseed canarygrass (Phalaris minor): A threat to wheat production in India

Littleseed canarygrass (Phalaris minor Retz.), a troublesome weed of wheat in India, has evolved multiple herbicide resistance across three modes of action: photosynthesis at the photosystem II site A, acetyl‐coA carboxylase (ACCase), and acetolactate synthase inhibition. The multiple herbicide‐resistant (MHR) populations had a low level of sulfosulfuron resistance but a high level of resistance to clodinafop and fenoxaprop (ACCase inhibitors). Some of the populations had GR₅₀ (50% growth reduction) values for clodinafop that were 11.7‐fold greater than that of the most susceptible population. The clodinafop‐resistant populations also showed a higher level of cross‐resistance to fenoxaprop (fop group) but a low level of cross‐resistance to pinoxaden (den group). Although clodinafop and pinoxaden are from two different chemical families (fop and den groups), their same site of action is responsible for cross‐resistance behavior. The populations that were resistant to four groups of herbicides (phenylureas, sulfonylurea, aryloxyphenoxypropionate, and phenylpyrazolin) were susceptible to the triazine (metribuzin and terbutryn) and dinitroaniline (pendimethalin) herbicides. The P. minor populations that were resistant to the aryloxyphenoxypropionate and phenylurea herbicides were effectively controlled by the sulfonylurea herbicide, sulfosulfuron. In the fields infested with P. minor that was resistant to clodinafop, a sulfosulfuron application (25 g ha^?1) increased the wheat yield by 99.2% over that achieved using the recommended rate of clodinafop (60 g ha^?1). However, the evolution of multiple resistance against the four groups is a threat to wheat production. To prevent the spread of MHR P. minor populations, as well as the extension of multiple resistance to new chemicals, concerted efforts in developing and implementing a sound, integrated weed management program are needed. The integrated approach, consisting of crop and herbicide rotation with cultural and mechanical weed control tactics, should be considered as a long‐term resistance management strategy that will help to sustain wheat productivity and farmers' income.     

A SNaPshot assay for the rapid and simple detection of known point mutations conferring resistance to ACCase‐inhibiting herbicides in Lolium spp.

Evolution of resistance to herbicides in weeds is becoming an increasing problem worldwide. To develop effective strategies for weed control, a thorough knowledge of the basis of resistance is required. Although non‐target‐site‐based resistance is widespread, target site resistance, often caused by a single nucleotide change in the gene encoding the target enzyme, is also a common factor affecting the efficacies of key herbicides. Therefore, fast and relatively simple high‐throughput screening methods to detect target site resistance mutations will represent important tools for monitoring the distribution and evolution of resistant alleles within weed populations. Here, we present a simple and quick method that can be used to simultaneously screen for up to 10 mutations from several target site resistance‐associated codons in a single reaction. As a proof of concept, this SNaPshot multiplex method was successfully applied to the genotyping of nine variable nucleotide positions in the CT domain of the chloroplastic ACCase gene from Lolium multiflorum plants from 54 populations. A total of 10 nucleotide substitutions at seven of these nine positions (namely codons 1781, 1999, 2027, 2041 2078, 2088 and 2096) are known to confer resistance to ACCase‐inhibiting herbicides. This assay has several advantages when compared with other methods currently in use in weed science. It can discriminate between different nucleotide changes at a single locus, as well as screening for SNPs from different target sites by pooling multiple PCR products within a single reaction. The method is scalable, allowing reactions to be carried out in either 96‐ or 384‐well plate formats, thus reducing work time and cost.     

An aspartate to glycine change in the carboxyl transferase domain of acetyl CoA carboxylase and non‐target‐site mechanism(s) confer resistance to ACCase inhibitor herbicides in a Lolium multiflorum population

BACKGROUND: The increasing use of ACCase‐inhibiting herbicides has resulted in evolved resistance in key grass weeds infesting cereal cropping systems worldwide. Here, a thorough and systematic approach is proposed to elucidate the basis of resistance to three ACCase herbicides in a Lolium multiflorum Lam. (Italian rye grass) population from the United Kingdom (UK24). RESULTS: Resistance to sethoxydim and pinoxaden was always associated with a dominant D2078G (Alopecurus myosuroides Huds. equivalent) target‐site mutation in UK24. Conversely, whole‐plant herbicide assays on predetermined ACCase genotypes showed very high levels of resistance to diclofop‐methyl for all three wild DD2078 and mutant DG2078 and GG2078 ACCase genotypes from the mixed resistant population UK24. This indicates the presence of other diclofop‐methyl‐specific resistance mechanism(s) yet to be determined in this population. The D2078G mutation could be detected using an unambiguous DNA‐based dCAPS procedure that proved very transferable to A. myosuroides, Avena fatua L., Setaria viridis (L.) Beauv. and Phalaris minor Retz. CONCLUSION: This study provides further understanding of the molecular basis of resistance to ACCase inhibitor herbicides in a Lolium population and a widely applicable PCR‐based method for monitoring the D2078G target‐site resistance mutation in five major grass weed species. Copyright © 2010 Society of Chemical Industry     

'Universal' primers for PCR-sequencing of grass chloroplastic acetyl-CoA carboxylase domains involved in resistance to herbicides

Primers were designed to amplify two regions involved in sensitivity to herbicides inhibiting the plastidic acetyl-CoA carboxylase (ACCase) from grasses (Poaceae). The first primer pair amplified a 551-bp amplicon containing a variable Ile/Leu codon at position 1781 in Alopecurus myosuroides sequence. The second primer pair amplified a 406-bp amplicon containing four variable codons (Trp/Cys, Ile/Asn, Asp/Gly, Gly/Ala) at positions 2027, 2041, 2078 and 2096, respectively, in A. myosuroides sequence. Both primer pairs amplified the targeted fragments from genes encoding plastidic ACCases, but not from the very similar genes encoding cytosolic ACCases. Clear DNA sequences were obtained from fresh or dried plant material from the field, and from 29 various grass species. Sequences revealed that the gene encoding plastidic ACCase in Poa annua and Festuca rubra contained a Leu₁₇₈₁ codon, in agreement with both species being inherently tolerant to herbicides inhibiting ACCase. Sequencing confirmed the hybrid origin of P. annua. Compared with ACCase enzyme assay, polymerase chain reaction is faster, can be performed from a single plant and suppresses the need for radioactive experiments. It can be completed with basic molecular biology laboratory equipment. It is the tool of choice for diagnosing resistance caused by alteration(s) of the plastidic ACCase.     

The response of ACCase-resistant Phalaris paradoxa populations involves two different target site mutations

Phalaris paradoxa (awned canary-grass) is an aggressive annual winter weed in wheat and other arable crops that is controlled mainly by ACCase-inhibiting herbicides: cyclohexanediones (DIMs), aryloxyphenoxypropionates (FOPs) and phenylpyrazolines (DENs, e.g. pinoxaden). The selection pressure imposed on the weed populations by repeated use of these herbicides has resulted in the evolution of increased numbers of ACCase-resistant populations of P. paradoxa in Israel and other countries. Two populations, Revadim (RV) and Mishmar Ha'emek (MH) that were exposed to differing weed and crop management tactics were investigated. Both populations were highly resistant to all FOPs, pinoxaden and cycloxydim, but responded differently to some DIMs. RV plants exhibited much higher resistance to tralkoxydim than MH plants, while showing similar low levels of resistance to tepraloxydim and clethodim. Both populations were equally susceptible to graminicides with other modes of action. The mutations responsible for the observed resistance were identified using PCR-RFLP and by sequencing the carboxyl transferase domain of the chloroplastic ACCase gene. RV plants possess a substitution of Asp₂₀₇₈ to Gly, whereas in MH population a mixture of Ile₂₀₄₁ to Asn or Asp₂₀₇₈ to Gly was found. Our study demonstrates that lack of herbicide and crop rotation may result in the evolution of diverse target site mutations and differential response of the whole plant to ACCase inhibitors.     

Diclofop‐resistant Lolium rigidum from northern Greece with cross‐resistance to ACCase inhibitors and multiple resistance to chlorsulfuron

Repeated use of ACCase‐ and ALS‐inhibiting herbicides in northern Greece has resulted in the evolution of a population of Lolium rigidum resistant to diclofop and chlorsulfuron. The biotype from Athos was highly resistant to diclofop and also exhibited differential cross‐resistance to clodinafop, fluazifop, tralkoxydim and sethoxydim. Assay of ACCase activity confirmed that the resistant biotype was tenfold more resistant to diclofop than the susceptible biotype, suggesting that the resistance mechanism could involve an altered target site. The diclofop‐resistant biotype has also exhibited multiple resistance to chlorsulfuron and the mechanism for this is unknown. Seed‐bioassay was found to be a rapid, cheap and reliable method to identify populations of L rigidum resistant to ACCase inhibitors and chlorsulfuron. Moreover, root elongation in the seed bioassay was more sensitive to ACCase inhibitors and chlorsulfuron than shoot elongation. © 2000 Society of Chemical Industry     

Cross-resistance patterns of winter wild oat (<Emphasis Type="Italic">Avena ludoviciana</Emphasis>) populations to ACCase inhibitor herbicides

The level of resistance and patterns of cross-resistance to clodinafop, sethoxydim, and pinoxaden were examined in 12 putative resistant and one susceptible populations of winter wild oat (Avena ludoviciana) collected from Fars Province, in the southwest of Iran. The responses of biomass and length of coleoptiles to the increasing dosages of the three herbicides were determined in both whole-plant and seed bioassays. In the whole-plant bioassay, all 12 putative resistant populations were found to be resistant to clodinafop with resistance ratios (R/S) ranging from 1.76 to >47.04. Most clodinafop-resistant populations exhibited low levels of cross-resistance to sethoxydim. Three highly sethoxydim-resistant populations, F2, S2, and ES4, were slightly resistant to clodinafop. Six populations (M1, M2, F2, S2, S4, and ES4) showed high cross-resistance to pinoxaden with R/S values as large as 10.73 to 40.29. A highly clodinafop-resistant population, M2, was more sensitive to pinoxaden than the susceptible population. The results of the seed bioassay resembled those obtained from the whole-plant experiment suggesting seed bioassay as an inexpensive, rapid method for screening-resistant genotypes.     

Characterisation of Avena fatua populations with resistance to multiple herbicides

Avena fatua (wild oat) populations with resistance (R) to one or more herbicides have been described in numerous cropping systems worldwide. We previously reported that the R3 and R4 wild oat populations from Montana, USA, were resistant to four herbicides representing three different modes of action: tralkoxydim [acetyl‐CoA carboxylase (ACCase] inhibitor), imazamethabenz and flucarbazone [acetolactate synthase (ALS) inhibitors] and difenzoquat (growth inhibitor). We now quantify resistance levels of these populations to triallate [very long chain fatty acid (VLCFA) biosynthesis inhibitor], pinoxaden (ACCase inhibitor) and paraquat (photosystem I inhibitor). Glasshouse dose–response experiments showed that, compared with the means of two susceptible (S) populations, the R3 and R4 populations were 17.5‐ and 18.1‐fold more resistant to triallate, 3.6‐ and 3.7‐fold more resistant to pinoxaden, respectively, and 3.2‐fold (R3) more resistant to paraquat. Pre‐treatment of R plants with the cytochrome P450 inhibitor malathion partially reversed the resistance phenotype for flucarbazone (both populations), imazamethabenz (R4), difenzoquat (R4) and pinoxaden (R3), but not for tralkoxydim, fenoxaprop‐P‐ethyl or triallate. Target site point mutations known to confer resistance to ALS or ACCase inhibitors were not detected via DNA sequencing and allele‐specific PCR assays in R plants, suggesting the involvement of non‐target site resistance mechanism(s) for these herbicides. Together, our results complete the initial characterisation of wild oat populations that are resistant to seven (R3) or six (R4) herbicides from five or four mode of action families respectively.     

Altered acetyl-coenzyme A carboxylase confers resistance to clethodim, fluazifop and sethoxydim in Setaria faberi and Digitaria sanguinalis

Summary Populations of Setaria faberi and Digitaria sanguinalis cross-resistant to sethoxydim and fluazifop-P-butyl were identified in a vegetable cropping system in Wisconsin, USA, in 1991 and 1992 respectively. Experiments were conducted with partially purified acetyl-CoA carboxylase (ACCase) to determine whether resistance to sethoxydim and other ACCase inhibitors in S. faberi and D. sanguinalis resulted from altered enzyme activity. Based on I₅₀ values (the herbicide dose that inhibited ACCase activity by 50% compared with untreated ACCase), ACCase of the resistant accession of S. faberi was 4.8-, 10.6- and 319-fold resistant to clethodim, fluazifop-P acid and sethoxydim, respectively, compared with that of the susceptible accession. Similarly, ACCase of the resistant accession of D. sanguinalis was 5.8-, 10.3- and 66-fold resistant to clethodim, fluazifop-P acid and sethoxydim respectively. These results indicated that resistance to ACCase inhibitors in these accessions of S. faberi and D. sanguinalis resulted from an altered ACCase enzyme that confers a very high level of resistance to sethoxydim.     

Cross-resistance profile of mesosulfuron-methyl-resistant Italian ryegrass in the southern United States

Diclofop-resistant Lolium species (ryegrass) is a major weed problem in wheat production worldwide. This study was conducted to determine the resistance pattern of diclofop-resistant ryegrass accessions from the southern United States to mesosulfuron-methyl, a recently commercialized herbicide for ryegrass control in wheat; to determine the cross-resistance pattern of a Lolium multiflorum Lam. (Italian ryegrass) accession, 03-1, to acetolactate synthase (ALS) and acetyl-CoA carboxylase (ACCase) inhibitors; and to determine the resistance mechanism of Italian ryegrass to mesosulfuron-methyl. Seventeen ryegrass accessions from Arkansas and Louisiana, including standard resistant and susceptible accessions, were used in this experiment. Fourteen of the 17 accessions were more resistant (four- to > 308-fold) to diclofop than the standard susceptible biotype. One accession, 03-1, was resistant to mesosulfuron-methyl as well as to other ALS inhibitor herbicides such as chlorsulfuron, imazamox and sulfometuron. Accession 03-1, however, did not show multiple resistance to the ACCase inhibitor herbicides diclofop, fluazifop, clethodim, sethoxydim and pinoxaden, nor to glyphosate. The in vivo ALS activity of the 03-1 biotype was less affected by mesosulfuron-methyl than the susceptible biotype. This indicates that the resistance mechanism of Italian ryegrass to mesosulfuron-methyl is partly due to an alteration in the target enzyme, ALS. It is concluded that diclofop-resistant ryegrass in the southern United States can be generally controlled by mesosulfuron-methyl. However, mesosulfuron-methyl must be used with caution because not all ryegrass populations are susceptible to it. There is a need for more thorough profiling of ryegrass resistance to herbicides.