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     

Mechanisms of resistance to acetyl-coenzyme A carboxylase inhibitors: a review

Resistance to acetyl-coenzyme A carboxylase (ACCase) inhibitors has developed in at least 10 grass weed species in recent years. In most instances, resistance is conferred by an ACCase alteration in the resistant biotypes that reduces sensitivity to aryloxyphenoxypropionate (AOPP) and cyclohexanedione (CHD) herbicides. Analysis of ACCase from many of these resistant weed biotypes suggests the presence of different mutations, each conferring a different pattern and level of resistance to various AOPP and CHD herbicides. In all cases analyzed to date, resistance is controlled by a single dominant or semi-dominant nuclear gene. In several weed biotypes, resistance is conferred by enhanced herbicide detoxification, primarily through elevated expression or activity of cytochrome P450 monooxygenase(s). This mechanism can confer cross-resistance to herbicides from other chemical classes with different modes of action. Finally, multiple herbicide resistance, i.e. the acquisition of several different resistance mechanisms, has been reported in some weed biotypes. ©1997 SCI     

Biochemical mechanisms of cross-resistance to aryloxyphenoxypropionate and cyclohexanedione herbicides in populations of Avena spp.

Aryloxyphenoxypropionate (APP) and cyclohexanedione (CHD) herbicides are used extensively in the UK to control grass weeds, including Avena spp. (wild-oats). Reports of resistance to APP and CHD herbicides are a particular concern for the agricultural community. In this study, the responses of four UK Avena populations were characterized towards the APP herbicides fenoxaprop-P-ethyl and fluazifop-P-butyl, and towards the CHD herbicides cycloxydim and tralkoxydim. An A. sterilis ssp. ludoviciana population (T/41) was found to be highly resistant to fenoxaprop-P-ethyl and fluazifop-P-butyl, but did not show cross-resistance to cycloxydim and tralkoxydim. In contrast, one A. sterilis ssp. ludoviciana (T/11) and one A. fatua population (Dorset) showed partial resistance to both APP herbicides and also showed cross-resistance to the CHD herbicide tralkoxydim, but not to cycloxydim. Before this study, the biochemical mechanisms that confer resistance to the APP and CHD herbicides in UK Avena populations were unknown. Results from the present study show that an enhanced rate of metabolism of fenoxaprop-P-ethyl was found to confer resistance in the two partially resistant Avena populations (T/11 and Dorset), and the presence of an insensitive form of the target enzyme, ACCase, was responsible for target site resistance to fenoxaprop-P-ethyl and fluazifop-P-butyl in the highly resistant population T/41. Cross-resistance to the CHD herbicide tralkoxydim in the T/11 and Dorset populations was not conferred by insensitive ACCase, and was most probably caused by enhanced metabolism. This is the first report that resistance to fenoxaprop-P-ethyl can be conferred by enhanced metabolism in Avena spp.     

PCR-based detection of resistance to acetyl-CoA carboxylase-inhibiting herbicides in black-grass (Alopecurus myosuroides Huds) and ryegrass (Lolium rigidum gaud)

A simple method based upon allele-specific PCR was developed to detect an isoleucine-leucine substitution in the gene encoding chloroplastic acetyl-coenzyme A carboxylase (ACCase) in two gramineous weeds: Lolium rigidum Gaud and Alopecurus myosuroides Huds. Analysis of 1800 A myosuroides and 750 L rigidum seedlings showed that the presence of ACCase leucine allele(s) conferred cross-resistance to the cyclohexanedione herbicide cycloxydim and to the aryloxyphenoxypropionate herbicides fenoxaprop-P-ethyl and diclofop-methyl. Seedlings containing ACCase leucine allele(s) could be either sensitive or resistant to the aryloxyphenoxypropionate herbicides haloxyfop-P-methyl and clodinafop-propargyl. Successful detection of resistant plants in a field population of A myosuroides was achieved using this PCR assay. Using it with basic molecular biology laboratory equipment, the presence of resistant leucine ACCase allele(s) can be detected within one working day.     

Differences in the molecular basis of resistance to the cyclohexanedione herbicide sethoxydim in Lolium multiflorum

Resistance to the cyclohexanedione (CHD) herbicide sethoxydim was investigated in two UK Lolium multiflorum populations, Yorks A2 and PYL. Resistance screening experiments demonstrated a qualitative difference in the responses of the two populations to sethoxydim, suggesting that the molecular basis of resistance between them was different. After treatment, Yorks A2 plants were either alive (78% of sample tested) or dead (22% tested) but plants of the PYL population showed two further intermediate categories of response. The level of acetyl-CoA carboxylase (ACCase) insensitivity directly correlated with the degree of resistance at the whole plant level, indicating that the molecular basis of resistance is associated with differences in ACCase sensitivity in each population. Direct sequencing of the carboxyl transferase domain of the ACCase gene showed that an Ile-418-Leu substitution in the L. multiflorum chloroplastic ACCase (GenBank accession number AY710293 ) confers resistance to sethoxydim in Yorks A2. This corresponds to amino acid residue 1781 in the Alopecurus myosuroides full ACCase sequence. This is the first report of this mutation in this L. multiflorum, which has also been reported in four other grass-weeds, including L. rigidum. However, no amino acid substitutions were found to be specifically associated with the resistant phenotypes in the PYL population and the molecular basis of resistance in this population remains to be resolved.     

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     

Resistance to ACCase-inhibiting herbicides and isoproturon in UK populations of Lolium multiflorum: mechanisms of resistance and implications for control

Herbicide-resistant Lolium multiflorum (Italian rye-grass) was first reported in the UK in 1993 and had been confirmed on 25 farms by 1999. In this study, resistance to five herbicides belonging to the aryloxyphenoxypropionate, cyclohexanedione and phenyl-urea classes was determined in six populations of L multiflorum from the UK under glasshouse and simulated field conditions. Glasshouse conditions tended to exaggerate the degree of resistance, but experiments performed in both environments detected resistance in four populations of L multiflorum. Four populations (Essex A1, Lincs A1, Wilts B1, Yorks A2) were resistant to diclofop-methyl, fluazifop-P-butyl, tralkoxydim and partially resistant to isoproturon, but only the population from Yorkshire (Yorks A2) showed resistance to cycloxydim. Biochemical analyses of acetyl coenzyme A carboxylase (ACCase) activity, oxygen consumption by thylakoids, diclofop metabolism and glutathione S-transferase activity showed that, in three of the resistant populations, an enhanced rate of herbicide metabolism conferred resistance. This is the first report world-wide of an enhanced metabolism mechanism of diclofop resistance in L multiflorum. In the Yorks A2 population, an insensitive ACCase was detected (target-site resistance) which also conferred cross-resistance to all of the other ACCase inhibitors investigated.     

Susceptibility of a broad-leaved weed, Acanthospermum hispidum, to the grass herbicide fluazifop-butyl

Broad-leaved plants are generally resistant to aryloxyphenoxypropionate (AOPP) and cyclohexanedione (CHD) herbicides. In laboratory experiments, however, we confirmed that Acanthospermum hispidum , a Compositae weed, was susceptible to one of the AOPP herbicides, fluazifop-butyl, but tolerant to other AOPP herbicides (quizalofop-ethyl and fenoxaprop-ethyl) and a CHD herbicide (sethoxydim). The symptoms induced by fluazifop-butyl in A. hispidum (wilting and necrosis) were distinctly different from those induced in oat (chlorosis). The period required to cause seedling death of A. hispidum (48–72 h) was shorter than that of oat ( ca 15 days). The ( R )-enantiomer of fluazifop-butyl was more active on this weed. In oat, lipid biosynthesis and acetyl-CoA carboxylase (ACCase) activity were inhibited, and electrolyte leakage from the shoots was increased by fluazifop-butyl and sethoxydim. In the case of A. hispidum , the membrane permeability increased and the lipid biosynthesis was inhibited only by fluazifop-butyl. These results indicate that A. hispidum is particularly sensitive to fluazifop-butyl, and its mechanism of action in the plant may be different from its mechanism of action in oat.     

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.     

Allelic variation of the ACCase gene and response to ACCase-inhibiting herbicides in pinoxaden-resistant Lolium spp

BACKGROUND: The repeated use of acetyl‐coenzyme A carboxylase (ACCase) inhibiting herbicides to control grass weeds has selected for resistance in Lolium spp. populations in Italy. The efficacy of pinoxaden, a recently marketed phenylpyrazoline herbicide, is of concern where resistance to ACCase inhibitors has already been ascertained. ACCase mutations associated with pinoxaden resistance were investigated, and the cross‐resistance pattern to clodinafop, haloxyfop, sethoxydim, clethodim and pinoxaden was established on homo/heterozygous plants for four mutant ACCase alleles. RESULTS: Seven different mutant ACCase alleles (1781‐Leu, 1999‐Leu, 2041‐Asn, 2041‐Val, 2078‐Gly, 2088‐Arg and 2096‐Ala) and 13 combinations with two types of mutation were detected in the pinoxaden‐resistant plants. The 1781‐Leu allele appears to confer a dominant resistance to pinoxaden, clodinafop, haloxyfop, sethoxydim and clethodim at 60 g AI ha^?1. The 2041‐Asn and 2041‐Val alleles are associated with dominant or partially dominant resistance to FOPs, no substantial resistance to DIMs and a moderate resistance to pinoxaden. The 2088‐Arg allele endows a partially dominant resistance to clodinafop, sethoxydim and most likely to pinoxaden. In addition, non‐target‐site resistance mechanisms seem to be involved in pinoxaden resistance. CONCLUSION: Almost all the ACCase mutations selected in the field by other ACCase inhibitors are likely to confer resistance to pinoxaden. Although pinoxaden is sometimes able to control FOP‐resistant populations, it should not be considered as a sustainable ACCase resistance management tool. The presence of non‐ACCase‐based resistance mechanisms that could confer resistance to herbicides with different modes of action further complicates the resistance management strategies. Copyright © 2011 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.     

直播稻田牛筋草对乙酰辅酶A羧化酶类除草剂抗性水平及其分子机制

为明确直播稻田牛筋草对乙酰辅酶A羧化酶 (ACCase) 类除草剂的抗药性水平及其抗性产生的分子机制,采用整株生物测定法测定了牛筋草对6种ACCase类除草剂的抗性水平,并分别对抗性种群和敏感种群的ACCase基因部分片段进行了扩增和测序。结果表明:疑似抗性种群SJ-1对唑酰草胺、氰氟草酯、精唑禾草灵、高效氟吡甲禾灵和烯禾啶产生了高水平抗性,其抗性倍数分别为56.6、62.5、128、52.0和16.3;对烯草酮产生了低水平抗性,相对抗性倍数为4.86。将抗性种群和敏感种群的ACCase基因片段序列进行比对分析发现,SJ-1种群ACCase基因2078位氨基酸由天冬氨酸 (GAT) 突变为甘氨酸 (GGT),该位点氨基酸突变可能是其对ACCase类除草剂产生抗药性的主要原因之一。     

小麦田大穗看麦娘对精噁唑禾草灵的抗性

为明确小麦田大穗看麦娘对精噁唑禾草灵的抗性水平及产生抗性的机理,采用整株法测定了河南省小麦田大穗看麦娘种群对精噁唑禾草灵的抗性水平,以及细胞色素P450s抑制剂胡椒基丁醚(PBO)对精噁唑禾草灵的增效作用,并通过基因测序技术研究了其靶标ACCase基因的突变位点。结果显示:与敏感种群HN-06相比,抗性种群HN-05对精噁唑禾草灵的抗性倍数为52.2,其ACCase基因存在Ile-2041-Asn和Gly-2096-Ala位点突变;喷施PBO后,精噁唑禾草灵对大穗看麦娘的GR50值(有效成分)为5.4 g/hm^2,表现出明显的增效作用,与未喷施PBO处理的差异倍数为161.3。研究表明,抗性种群HN-05对精噁唑禾草灵已产生高水平抗性,该抗性的产生可能是由于其靶标基因突变和P450s介导的代谢增强同时导致的,即表现出了靶标抗性和非靶标抗性共存的现象。     

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.     

Tolerance to acetolactate synthase and acetyl-coenzyme A carboxylase inhibiting herbicides in Vulpia bromoides is conferred by two co-existing resistance mechanisms

Vulpia bromoides is a grass species naturally tolerant to acetolactate synthase (ALS) and acetyl-coenzyme A carboxylase (ACCase) inhibiting herbicides. The mechanism of tolerance to ALS herbicides was determined as cytochrome P450-monooxygenase mediated metabolic detoxification. The ALS enzyme extract partially purified from V. bromoides shoot tissue was found to be as sensitive as that of herbicide susceptible Lolium rigidum to ALS-inhibiting sulfonylurea (SU), triazolopyrimidine (TP), and imidazolinone (IM) herbicides. Furthermore, phytotoxicity of the wheat-selective SU herbicide chlorsulfuron was significantly enhanced in vivo in the presence of the known P450 inhibitor malathion. In contract, the biochemical basis of tolerance to ACCase inhibiting herbicides was established as an insensitive ACCase. In vitro ACCase inhibition assays showed that, compared to a herbicide susceptible L. rigidum, the V. bromoides ACCase was moderately (4.5- to 9.5-fold) insensitive to the aryloxyphenoxypropionate (APP) herbicides diclofop, fluazifop, and haloxyfop and highly insensitive (20- to >71-fold) to the cyclohexanedione (CHD) herbicides sethoxydim and tralkoxydim. No differential absorption or de-esterification of fluazifop-P-butyl was observed between the two species at 48 h after herbicide application, and furthermore V. bromoides did not detoxify fluazifop acid as rapidly as susceptible L. rigidum. It is concluded that two co-existing resistance mechanisms, i.e., an enhanced metabolism of ALS herbicides and an insensitive target ACCase, endow natural tolerance to ALS and ACCase inhibiting herbicides in V. bromoides.     

Mechanisms of Resistance to Aryloxyphenoxypropionate Herbicides in Two Resistant Biotypes ofAlopecurus myosuroides(blackgrass): Herbicide Metabolism as a Cross-Resistance Mechanism

The mechanisms of AOPP herbicide resistance in twoAlopecurus myosuroidesbiotypes were investigated. Resistant biotype Peldon A1, which is highly resistant to the phenyl-urea chlorotoluron, is moderately resistant to the AOPP herbicides diclofop-methyl, fenoxaprop-ethyl, fluazifop-P-butyl, and the CHD tralkoxydim. Resistant biotype Lincs. E1, which is only moderately resistant to chlorotoluron, is highly resistant to the AOPP herbicide fenoxaprop-ethyl, and moderately resistant to diclofop-methyl, fluazifop-P-butyl, and the CHD tralkoxydim. There is no clear evidence of resistance to the CHD sethoxydim in either biotype. Both Peldon A1 and Lincs. E1 exhibited moderately enhanced metabolism of diclofop-methyl. The approximate half life of diclofop was 8 and 9 HAT, respectively, compared to 17 HAT for the susceptible Rothamsted biotype. Peldon A1 showed moderately enhanced metabolism of fenoxaprop-P-ethyl. However, in the highly resistant Lincs. E1, fenoxaprop-P-ethyl metabolism rates were intermediate between Peldon A1 and the susceptible biotype. Fenoxaprop-P-ethyl metabolism inA. myosuroideswas not significantly reduced by inhibitors of cytochrome P450: PBO, tetcyclasis, or ABT. While enhanced herbicide metabolism can account for the moderate AOPP/CHD resistance observed in Peldon A1in vivo, it cannot account in total for fenoxaprop-ethyl resistance in Lincs. E1. Lincs. E1 may possess one or more additional resistance mechanism.     

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.     

Modelling different cultivation and herbicide strategies for their effect on herbicide resistance in Alopecurus myosuroides

A single dominant mutation conferring resistance to aryloxyphenoxypropionate (AOPP) and cyclohexanedione (CHD) herbicides was incorporated into a quantitative model for the population development of Alopecurus myosuroide s Huds. The model predicts that from an initial seedbank of 100 seed m^–2, 10^–6 of which mutate to resistance each generation, and annual use of AOPP/CHD herbicides which kill 90% of susceptible but no resistant plants, a threshold of 10 plants m^–2 surviving herbicides ('field resistance') will develop: in 9–10 years if all tillage is by tine cultivation to 10 cm deep; after 28–30 years of annual ploughing; in 12 years if tine cultivations are interspersed with ploughing once every 4 years. If AOPP/CHD herbicides are alternated with herbicides with different modes of action, outcomes depend on the annual kill rate: with 95% kill (of susceptible plants by AOPP/CHDs and all plants by alternative herbicides) and tine cultivation, field resistance develops in 22 years; however, resistance can be delayed for 45 years if AOPP/CHDs are rotated with two additional herbicides, each with a different mode of action. The model predictions on the number of years required for field resistance to develop are not highly sensitive to the density of the seedbank or the initial frequency of resistance.     

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