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     

Sulfonylurea herbicide-resistant Monochoria vaginalis in Korean rice culture

Nine Monochoria vaginalis Pres1 accessions from Chonnam province, Korea were tested for resistance to the sulfonylurea herbicide, imazosulfuron, in whole-plant response bioassay. All accessions were confirmed resistant (R) to imazosulfuron. The GR50 (imazosulfuron concentration that reduced shoot dry weight by 50%) values of R accessions were 1112-3172 (accession #9) times higher than that of the standard susceptible (S) accession. Accession #9 exhibited cross-resistance to other sulfonylurea herbicides, bensulfuron-methyl, cyclosulfamuron and pyrazosulfuron-ethyl, but not to the imidazolinone herbicides, imazapyr and imazaquin. The R biotype could be controlled by other herbicides with different modes of action, such as mefenacet and pyrazolate, applied to soil at recommended rates. Foliar-applied herbicides, 2,4-D and bentazone, also controlled both the R and S biotypes. Sulfonylurea-based mixtures, except ethoxysulfuron plus fentrazamide, did not control resistant M. vaginalis. Rice yield was reduced 70% by resistant M. vaginalis that escaped pyrazosulfuron-ethyl plus molinate, compared with hand weeding in direct-seeded rice culture. In contrast, rice yield was reduced 44% by resistant M. vaginalis that survived the pyrazosulfuron-ethyl plus molinate treatment, compared with pyrazolate plus butachlor in transplanted rice culture. In vitro acetolactate synthase (ALS) activity of the R biotype was 183, 35, 130 and 31 times more resistant to imazosulfuron, bensulfuron-methyl, cyclosulfamuron and pyrazosulfuron-ethyl, respectively, than the S biotype. Imidazolinone herbicides, imazapyr and imazaquin had similar effect on in vitro ALS activity of the R and S biotypes. The in vivo ALS activity of the R biotype was also less affected than the S biotype by the sulfonylurea herbicides imazosulfuron and pyrazosulfuron-ethyl. Results of in vitro and in vivo ALS assays indicate that the resistance mechanism of M. vaginalis to sulfonylurea herbicides may be due, in part, to an alteration in the target enzyme, ALS. Since the level of resistance in the enzyme assay was much lower than that in the whole-plant assay, other mechanisms of resistance, such as herbicide metabolism, may be involved.     

河南省多花黑麦草对ACCase和ALS抑制剂的抗性及其靶标基因突变分析

为明确河南省部分地区的多花黑麦草Lolium multiflorum种群对乙酰辅酶A羧化酶（acetylCoA carboxylase,ACCase）和乙酰乳酸合成酶（acetolactate synthase,ALS）抑制剂类除草剂的抗性水平和抗性机理,采用整株生物测定法测定采自新乡市和驻马店市的多花黑麦草种群对ACCase抑制剂类除草剂精噁唑禾草灵、炔草酯、唑啉草酯和ALS抑制剂类除草剂甲基二磺隆、氟唑磺隆、啶磺草胺的抗性水平,并对多花黑麦草ACCase和ALS靶标酶编码基因进行克隆及氨基酸序列比对,分析其靶标抗性机理。结果显示,与多花黑麦草敏感种群HNXX01相比,HNZMD04和HNXX05种群对6种除草剂均产生了抗性,HNZMD04种群对精噁唑禾草灵和啶磺草胺的相对抗性倍数分别为44.65和40.31,对炔草酯和氟唑磺隆的相对抗性倍数分别为11.91和11.93;HNXX05种群对精噁唑禾草灵和氟唑磺隆的相对抗性倍数分别为27.70和25.67。HNZMD04和HNXX05抗性种群的ACCase基因均发生了D2078G突变,2个种群的突变率分别为55%和70%;HNZMD04...     

Molecular characterization and inheritance of resistance to ACCase-inhibiting herbicides in Lolium rigidum

The molecular basis and mode of inheritance of resistance to ACCase-inhibiting herbicides were investigated in a biotype of Lolium rigidum Gaud that has been discovered in Israel. Dose-response experiments at the whole-plant level have revealed that the resistant biotype was more resistant (6.3- to 40-fold) than the susceptible wild-type to ACCase-inhibiting herbicides. A 276-bp genomic DNA encoding the carboxyltransferase domain within the chloroplastic ACCase from resistant and susceptible biotypes were amplified by PCR and analyzed. Sequence comparison revealed that a single isoleucine-to-leucine substitution differentiated ACCases from susceptible and resistant biotypes (corresponds to residue 1769 of wheat ACCase, Acc No AF029895). A PCR amplification of specific alleles (PASA) method was developed to detect the allele composition leading to isoleucine-leucine mutation. ACCase extracted from homozygote resistant, heterozygote and homozygote susceptible plants showed IC50 values of 25.8, 5.6 and 0.6 microM, respectively, suggesting that alteration in the ACCase is governed by a co-dominant gene. The inheritance studies confirmed that the resistance of L rigidum to ACCase-inhibiting herbicides is governed by a single, nuclear and co-dominant gene.     

Multiple herbicide‐resistant Lolium rigidum (annual ryegrass) now dominates across the Western Australian grain belt

Lolium rigidum (annual or rigid ryegrass) is a widespread annual weed in cropping systems of southern Australia, and herbicide resistance in L. rigidum is a common problem in this region. In 2010, a random survey was conducted across the grain belt of Western Australia to determine the frequency of herbicide‐resistant L. rigidum populations and to compare this with the results of previous surveys in 1998 and 2003. During the survey, 466 cropping fields were visited, with a total of 362 L. rigidum populations collected. Screening of these populations with the herbicides commonly used for control of L. rigidum revealed that resistance to the ACCase‐ and ALS‐inhibiting herbicides was common, with 96% of populations having plants resistant to the ACCase herbicide diclofop‐methyl and 98% having plants resistant to the ALS herbicide sulfometuron. Resistance to another ACCase herbicide, clethodim, is increasing, with 65% of populations now containing resistant plants. Resistance to other herbicide modes of action was significantly lower, with 27% of populations containing plants with resistance to the pre‐emergent herbicide trifluralin, and glyphosate, atrazine and paraquat providing good control of most of the populations screened in this survey. Ninety five per cent of L. rigidum populations contained plants with resistance to at least two herbicide modes of action. These results demonstrate that resistance levels have increased dramatically for the ACCase‐ and ALS‐inhibiting herbicides since the last survey in 2003 (>95% vs. 70–90%); therefore, the use of a wide range of integrated weed management options are required to sustain these cropping systems in the future.     

Amaranthus palmeri resistance and differential tolerance of Amaranthus palmeri and Amaranthus hybridus to ALS-inhibitor herbicides

Suspected imazaquin-resistant accessions of Amaranthus palmeri were studied to determine the magnitude of resistance and cross-resistance to acetolactate synthase (ALS)-inhibiting herbicides and compare differential tolerance of A palmeri and Amaranthus hybridus to ALS inhibitors. Five of seven A palmeri accessions were resistant to imazaquin. The most imazaquin-resistant accession, accession 7, also showed 74, 39 and 117 times higher resistance than the susceptible biotype to chlorimuron, diclosulam and pyrithiobac, respectively. Resistance to imazaquin and cross-resistance to other ALS inhibitors in A palmeri was due to a less-sensitive ALS enzyme. A palmeri was 70 times more tolerant to imazaquin than A hybridus. A palmeri was also seven times more tolerant to pyrithiobac than A hybridus. Differences in ALS enzyme sensitivity could not fully account for the high tolerance of A palmeri to imazaquin compared to A hybridus. Both species were equally affected by chlorimuron and diclosulam.     

Cross-resistance pattern and alternative herbicides for Cyperus difformis resistant to sulfonylurea herbicides in Korea

A Cyperus difformis L accession from Chonnam province, Korea was tested for resistance to the sulfonylurea herbicide, imazosulfuron. The accession was confirmed to be resistant (R) and was cross-resistant to other sulfonylurea herbicides, bensulfuron-methyl, cyclosulfamuron and pyrazosulfuron-ethyl, the pyrimidinyl thiobenzoate herbicide, bispyribac-sodium, and the imidazolinone herbicide imazapyr, but not to imazaquin. Multiple resistance was tested using twelve herbicides with target sites other than acetolactate synthase (ALS). The R biotype could be controlled by other herbicides with different modes of action such as butachlor, carfentrazone-ethyl, clomeprop, dithiopyr, esprocarb, mefenacet, oxadiazon, pretilachlor, pyrazolate and thiobencarb, applied to soil at recommended rates. Several sulfonylurea herbicide-based mixtures can control both the R and S biotypes of C difformis, except sulfonylurea plus dimepiperate, molinate or pyriftalid, and pyrazolate plus butachlor. Although mixtures of sulfonylurea herbicides might be more effective, they should be avoided and used only in special cases. In terms of in vitro ALS activity, the R biotype was 1139-, 3583-, 1482-, 416-, 5- and 9-fold more resistant to bensulfuron-methyl, cyclosulfamuron, imazosulfuron, pyrazosulfuron-ethyl, bispyribac-sodium and imazapyr, respectively, than the S biotype. The in vivo ALS activity of the R biotype was also less affected by the sulfonylurea herbicides, imazosulfuron and pyrazosulfuron-ethyl, than the S biotype. Results of in vitro and in vivo ALS assays indicated that the resistance mechanism of C difformis to ALS inhibitor herbicides was primarily due to an alteration in the target enzyme, ALS. Greenhouse experiments showed delayed flowering and reduced seed production of the R biotype, which could possibly result in reduced fitness. This unusual observation needs to be confirmed in field situations.     

Resistance to diclofop-methyl in two Lolium spp. populations from Italy: studies on the mechanism of resistance

The mechanisms of herbicide resistance were investigated in two diclofop-methyl-resistant Lolium spp. populations from central Italy, Roma '94 and Tuscania '97. These two populations were compared with two susceptible Italian populations (Vetralla '94, Tarquinia '97) and a resistant and a susceptible population from Australia, SLR31 and VLR1. The activity of acetyl Co-A carboxylase (ACCase) extracted from susceptible (S) or resistant (R) individuals from the Italian populations was inhibited by both aryloxyphenoxypropanoate (diclofop acid and fluazifop acid) and cyclohexanedione (sethoxydim) herbicides. Diclofop-methyl was rapidly de-esterified to diclofop acid at a similar rate in both R and S populations. In all populations, diclofop acid was subsequently degraded to other metabolites. The rate of degradation of diclofop acid was not significantly faster in R than in S populations; however, diclofop acid was degraded more completely in Roma '94 and Tuscania '97 compared with the S populations. Application of the mixed-function oxidase inhibitor 1-aminobenzotriazole (ABT) significantly enhanced diclofop-methyl toxicity towards both R populations, but not in S populations. However, enhanced herbicide metabolism does not completely account for the measured resistance level. A mechanism other than an altered ACCase and enhanced herbicide metabolism appears to be responsible for resistance to diclofop-methyl in Roma '94 and Tuscania '97.     

Confirmed resistance to aryloxyphenoxypropionate herbicides in Phalaris minor populations in Iran

Phalaris minor (littleseed canary grass) is a major weed in wheat fields in some parts of Iran. Diclofop‐methyl, fenoxaprop‐P‐ethyl, and clodinafop‐propargyl are three acetyl coenzyme A carboxylase (ACCase)‐inhibiting herbicides that are commonly used to control this grass in wheat fields. Thirty‐four P. minor populations with suspected resistance to ACCase‐inhibiting herbicides were sampled from wheat fields in the provinces of Fars and Golestan in Iran. The dose–response assays that were conducted under controlled greenhouse conditions indicated that 14 populations were resistant to fenoxaprop‐P‐ethyl, seven populations were resistant to both fenoxaprop‐P‐ethyl and diclofop‐methyl, and three populations were resistant to fenoxaprop‐P‐ethyl, diclofop‐methyl, and clodinafop‐propargyl. These populations showed different levels of resistance to the applied herbicides, compared to the susceptible population. These results suggest that different mechanisms of resistance could be involved. The enzyme assay revealed that the existence of modified ACCase in the three most‐resistant populations (AR, MR4, and SR3) is responsible for the resistance of these populations.     

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.     

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.     

小麦田看麦娘对甲基二磺隆的抗性水平及分子机制初探

看麦娘是中国长江中下游地区稻茬麦田的主要恶性杂草之一,甲基二磺隆是防治小麦田看麦娘等禾本科杂草的重要除草剂.该研究团队前期在安徽省凤台县小麦田采集到疑似抗性种群看麦娘(AHFT-01),为明确其对甲基二磺隆的抗性发生情况及潜在的抗性机制,采用温室盆栽法在整株水平上测定了该种群对甲基二磺隆及其他乙酰乳酸合成酶(ALS)抑...     

Contamination of internationally traded wheat by herbicide‐resistant Lolium rigidum

As herbicide‐resistant weeds have spread in the agricultural fields of grain‐exporting countries, their seeds could be introduced into other countries as contaminants in imported grain. The spread of resistance genes through seed and pollen can cause significant economic loss. In order to assess the extent of the problem, we investigated the contamination by herbicide‐resistant annual ryegrass (Lolium rigidum) of wheat imported from Western Australia into Japan. Annual ryegrass seeds were recovered from wheat shipments and seed bioassays were conducted to identify resistance to the herbicides that are commonly used in Australia: diclofop‐methyl, sethoxydim, chlorsulfuron, and glyphosate. Nearly 4500 ryegrass seeds were detected in 20 kg of wheat that was imported in both 2006 and 2007. About 35% and 15% of the seeds were resistant to diclofop‐methyl, 5% and 6% were resistant to sethoxydim, and 56% and 60% were resistant to chlorsulfuron in 2006 and 2007, respectively. None was resistant to glyphosate in either year. As the contamination of crops by herbicide‐resistant weeds is probably a common phenomenon, the monitoring of incoming grain shipments is necessary to stem the further spread of herbicide‐resistant weeds into importing countries.     

A Diclofop-methyl-Resistant Avena sterilis Biotype with a Herbicide-Resistant Acetyl-coenzyme A Carboxylase and Enhanced Metabolism of Diclofop-methyl

An Avena sterilis biotype was found to be highly resistant to aryloxyphenoxypropionate (APP) herbicides, especially diclofop-methyl. At the enzyme level, this biotype contained a modified acetyl-coenzyme A carboxylase (ACCase) with six-fold resistance to diclofop acid. Absorption and translocation of [¹⁴C]diclofop-methyl applied to the leaf axil of the two-leaf stage plants were similar in both susceptible and resistant biotypes. However, the rate of metabolism of [¹⁴C]diclofop was increased 1·5-fold in this resistant biotype compared to the susceptible. Experiments with tetcyclacis, a cytochrome P450 monooxygenase inhibitor, indicated that inhibition of this enhanced diclofop metabolism increased diclofop-methyl phytotoxicity in this biotype. Studies with ten individual families of the resistant biotype indicated that both mechanisms of resistance, an altered target site and enhanced metabolism, are present in each individual of the population. Hence, it is likely that these two mechanisms of resistance both contribute to resistance in this biotype. © 1997 SCI.     

Resistance of Camelina microcarpa to acetolactate synthase inhibiting herbicides

An accession of Camelina microcarpa suspected to be resistant to sulfonylurea herbicides was identified in Oregon in 1998 field experiments. Greenhouse research confirmed that the putative resistant biotype was resistant to chlorsulfuron and metsulfuron on a whole plant level. Compared with the resistant (R) biotype, the susceptible (S) biotype was 1000 and 10 000‐fold more sensitive to metsulfuron and chlorsulfuron respectively. The R biotype was also resistant to other sulfonylurea, sulfonylaminocarbonyl‐triazolinone, imidazolinone and triazolopyrimidine herbicides. An in vivo enzyme assay indicated that acetolactate synthase (ALS) from the R plants required 111 times more chlorsulfuron to inhibit activity by 50% compared with the amount required to have a similar effect on ALS from S plants. Analysis of the nucleotide and amino acid sequences demonstrated that a single‐point mutation from G to T in the als1 gene conferred the change from the amino acid tryptophan to leucine at position 572 in the resistant biotype. This research confirmed that ALS inhibitor resistance in an Oregon accession of C. microcarpa is based on an altered target site conferred by a single‐point mutation.     

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     

Growth and yield responses of Italian ryegrass (Lolium multiflorum) to diclofop-methyl and ozone

We evaluated the combined effects of diclofop‐methyl herbicide application and the air pollutant ozone (O₃) on diclofop‐methyl‐resistant and ‐susceptible biotypes of Italian ryegrass (Lolium multiflorum). We conducted two experiments, one with a long vegetative growth period and the other with a short vegetative growth in late spring with seed production in summer. As expected, because of its phytotoxicity, the herbicide alone reduced total vegetative biomass, leaf area, tiller number and seed production at most sampling periods in susceptible plants for both experiments. However, it had variable effects on resistant plants, including a positive effect on seed production. Ozone alone delayed vegetative biomass accumulation and reduced leaf area and seed biomass in both experiments. However, the effects of O₃ on some parameters were altered by herbicide rate and/or biotype. Especially notable was a greater reduction in seed biomass because of O₃ in resistant than in susceptible plants with no herbicide. If these apparent differential responses to herbicide and O₃ stress of susceptible and resistant plants are confirmed and persist over time, evolutionary tradeoffs may occur. For example, the frequency of resistant plants in a population may be altered in response to interactions between herbicides and other anthropogenic stresses.     

Diclofop-methyl resistance in populations of Lolium spp. from central Italy

Populations of Lolium spp. collected in central Italy were screened for resistance to acetyl-coenzyme A carboxylase (ACCase)-inhibiting herbicides and compared with known susceptible and resistant Lolium rigidum (Gaud.) populations from Australia. Populations Roma'94 and Tuscania'97 were up to 8- and 7.5-fold more resistant to diclofop-methyl, respectively, than susceptible populations in pot experiments. However, populations Tarquinia'97 and Vetralla'94 were not resistant. Diclofop-methyl resistance levels in the Italian populations were lower than in the Australian populations SLR31 and WLR96 (16.5 and > 64 times more resistant than S respectively). In an agar germination test, Tuscania'97 showed low levels of cross-resistance to fluazifop-p-butyl, whereas no cross-resistance was found in the Roma'94 population.     

A rapid reliable test for screening aryloxyphenoxy- propionic acid resistance within Alopecurus myosuroides and Lolium spp. populations

A reliable seedling bioassay was developed and tested for the rapid screening for resistance to aryloxyphenoxypropionic (APP) herbicides in Alopecurus myosuroides and Lolium spp. populations. It is based upon the difference in coleoptile length of resistant and susceptible A. myosuroides and Lolium seedlings, respectively, exposed to fenoxaprop-P acid and diclofop acid solution for 6 days in a plastic box. A 6 mg L⁻¹ fenoxaprop-P acid solution was selected as the best concentration for a reliable screening of resistant biotypes within A. myosuroides populations. At this concentration, coleoptile lengths of susceptible and resistant seedlings were shorter and longer than 10 mm respectively. Similarly, resistant seedlings within Lolium populations were easily detected at 10 mg L⁻¹ diclofop acid. At this concentration, coleoptile lengths of susceptible and resistant seedlings were shorter and longer than 20 mm respectively. For both populations, the coleoptile length distributions appear to discriminate between two kinds of APP-resistant biotypes (highly and slightly resistant).     

Characterisation of target-site resistance to ACCase-inhibiting herbicides in the weed Alopecurus myosuroides (black-grass)

Resistance to aryloxyphenoxypropionate (AOPP), cyclohexanedione (CHD) and phenylurea herbicides was determined in UK populations of Alopecurus myosuroides Huds. Two populations (Oxford AA1, Notts. A1) were highly resistant (Resistance indices 13-->1000) to the AOPP and CHD herbicides fenoxaprop, diclofop, fluazifop-P and sethoxydim, but only marginally resistant to the phenylurea, chlorotoluron. Analyses of acetyl coenzyme A carboxylase (ACCase) activity showed that an insensitive ACCase conferred resistance to all the AOPP/CHD herbicides investigated. Another population, Oxford S1, showed no resistance to sethoxydim at the population level, but contained a small proportion of plants (<10%) with an insensitive ACCase. Genetic studies on the Notts A1 and Oxford S1 populations demonstrated that target site resistance conferred by an insensitive ACCase is monogenic, nuclearly inherited with the resistant allele showing complete dominance. Investigations of the molecular basis of resistance in the Notts A1 population showed that sethoxydim resistance in A myosuroides was associated with the substitution of an isoleucine in susceptible with a leucine in resistant plants, which has also been found in three other resistant grass-weed species (Setaria viridis (L) Beauv, Avena fatua L, Lolium rigidum Gaud).