Littleseed canarygrass (Phalaris minor) resistance to clodinafop‐propargyl in wheat fields in north‐western India: Appraisal and management

Littleseed canarygrass (～canarygrass) evolved populations that are resistant to isoproturon during the early 1990s in north‐western India. Clodinafop‐propargyl (～clodinafop) was recommended for controlling these populations. It has been used extensively in wheat for the last several years. Recently, poor or no control of canarygrass by clodinafop has been observed in large areas, which could be related to cross‐resistance or multiple resistance. This study was designed to test whether resistance has evolved in canarygrass populations against clodinafop and to explore control of the resistant populations with sulfosulfuron and pinoxaden. Among the 311 canarygrass populations that were tested, 86, 55 and 34 showed variable phytotoxicity (0–99%) due to 0.030, 0.060 and 0.120 kg ha^?1 clodinafop, respectively. Based on the resistance index, 11 populations were “highly resistant”, 60 were “resistant” and the rest (240) were “susceptible” to clodinafop. Five and six clodinafop‐resistant populations showed slight resistance to 0.0125 kg ha^?1 sulfosulfuron and 0.025 kg ha^?1 pinoxaden, respectively. But, sulfosulfuron at 0.025 and 0.050 kg ha^?1 and pinoxaden at 0.050 and 0.100 kg ha^?1 controlled all the canarygrass populations. Clodinafop used for 4 years increased the chance of resistance evolving, whereas its rotation with sulfosulfuron reduced the chance of resistance evolving. This study showed that considerable canarygrass populations have evolved a low‐to‐high degree of resistance against clodinafop. The further use of clodinafop would lead to the spread of resistance in larger areas through the dispersal of resistant seeds. Clodinafop should be replaced with 0.025 kg ha^?1 sulfosulfuron or 0.050 kg ha^?1 pinoxaden. Besides, where canarygrass has not evolved resistance, the yearly rotation of sulfosulfuron with clodanafop or pinoxaden might delay the evolution of resistance.     

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     

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 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.     

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。     

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.     

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     

湖南省部分地区棉田牛筋草(Eleusine indica)对精喹禾灵的抗性

采用整株法测定了湖南省部分地区棉田牛筋草(Eleusine indica)对精喹禾灵的抗性水平,还测定了精喹禾灵对牛筋草抗(R)、感(S)种群体内GSTs及SOD、POD、CAT影响的差异。整株法测定结果显示,相对于敏感的南县种群,其他地区棉田牛筋草对精喹禾灵的抗性指数在1.6~9.7之间,其中湘阴种群最高为9.7,澧县种群最低为1.6;精喹禾灵处理2d后,R种群GSTs活性急剧上升,在第3天达到最高,随后急剧下降,5d之后趋于平缓。S种群GSTs活性在施药后先上升后下降。药剂处理后,R种群的SOD和POD活性在中期显著低于S种群,R、S种群的CAT活性在药后第9天有明显差异。结果表明,R种群对精喹禾灵产生抗性的原因可能是GSTs对精喹禾灵的代谢作用加强,抗氧化酶系活性的变化可能与抗性相关。     

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.     

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.     

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.     

抗精噁唑禾草灵的日本看麦娘ACCase基因突变

为明确日本看麦娘抗性种群对精噁唑禾草灵的抗性水平及抗性产生的分子机制,采用整株水平测定法测定了日本看麦娘对精噁唑禾草灵的抗性水平,扩增和比对了日本看麦娘抗性和敏感种群间乙酰辅酶A羧化酶(acetyl-Co A carboxylase,ACCase)基因的差异。结果显示,与敏感种群AH-7相比,抗性种群AH-25对精噁唑禾草灵的抗性倍数为33.82;AH-25种群ACCase基因CT区域2 078位氨基酸发生了突变,由天冬氨酸GAT突变为甘氨酸GGT;AH-25种群对炔草酯、烯草酮和烯禾啶产生了高水平的抗性,抗性倍数分别为35.66、38.64和29.14,对高效氟吡甲禾灵产生了低水平的抗性,抗性倍数为3.04,对精喹禾灵和唑啉草酯较敏感。表明ACCase基因2 078位氨基酸的突变可能是导致精噁唑禾草灵产生高水平抗性的重要原因。     

黑龙江省稻田野慈姑对丙嗪嘧磺隆抗性相关研究

通过整株盆栽法研究黑龙江省佳木斯市汤原县(种群R1)、856农场(种群R2)、密山市(种群R3)3个水稻田野慈姑种群对丙嗪嘧磺隆的抗性水平,采用分子生物学技术分析3个野慈姑种群在靶标酶基因上的差异,确定3个野慈姑种群对丙嗪嘧磺隆和苄嘧磺隆是否存在交互抗性。结果显示,黑龙江R1、R2、R3种群抗性指数(RI)分别为11.92、22.68、35.99。与敏感的七台河种群S相比,R1、R2、R3的ALS基因均在Pro_(197)位发生不同突变。R1种群为Thr_(197)取代了Pro_(197);R2、R3种群为Ser_(197)取代了Pro_(197),ALS基因的突变是其产生抗性的主要原因。3个野慈姑种群对丙嗪嘧磺隆和苄嘧磺隆存在交互抗性。     

山东省部分市县麦田杂草麦家公Lithospermum arvense对苯磺隆的抗药性

采用温室盆栽法和培养皿法测定了山东省部分市县冬小麦田杂草麦家公Lithospermum arvense L.对苯磺隆的抗药性水平,以及其抗药性生物型乙酰乳酸合成酶(ALS)对苯磺隆的敏感性。温室盆栽结果显示,供试杂草对苯磺隆产生了不同程度的抗药性,其中胶州麦家公生物型抗性水平最高,抗性倍数为12.8倍;培养皿法测定结果也显示胶州麦家公生物型抗性水平最高,但抗性倍数为3.89倍。交互抗性测定结果表明,胶州抗性麦家公生物型对其他ALS抑制剂噻吩磺隆和苄嘧磺隆已产生不同程度的交互抗性,其中对噻吩磺隆的抗性倍数达到3.11倍。离体条件下,与敏感生物型ALS活力的抑制中浓度(IC50)相比较,胶州抗性麦家公生物型的IC50值是敏感麦家公的 2.65倍。表明ALS敏感性降低可能是山东部分市县麦家公对苯磺隆产生抗药性的重要原因之一。     

Inheritance of resistance in <Emphasis Type="Italic">Solanum nigrum</Emphasis> to <Emphasis Type="Italic">Phytophthora infestans</Emphasis>

Solanum nigrum, black nightshade, is a wild non-tuber bearing hexaploid species with a high level of resistance to Phytophthora infestans (Colon et al. 1993), the causal agent of potato late blight, the most devastating disease in potato production. However, the genetic mode of resistance in S. nigrum is still poorly understood. In the present study, two S. nigrum accessions, 984750019 (N19) and #13, resistant (R) and susceptible (S), respectively, to three different isolates of P. infestans, were sexually crossed. The various kinds of progeny including F1, F2, F3, and backcross populations (BC₁; F1 × S), as well as two populations produced by self-pollinating the R parent and S parent, were each screened for susceptibility to P. infestans isolate MP 324 using detached leaf assays. Fifty seedling plant individuals of the F1 progeny were each resistant to this specific isolate, similarly to the seedling plants resulting from self-pollination of the resistant R parent. Thirty seedling plants obtained from self-pollination of the S parent were susceptible. Among a total of 180 F2 plants, the segregation ratio between resistant and susceptible plants was approximately 3: 1. Among the 66 seedling plants of the BC₁ progeny originating from crossing an F1 plant with the susceptible S parent, there were 26 susceptible and 40 resistant plants to P. infestans. The segregation patterns obtained indicated monogenic dominant inheritance of resistance to P. infestans isolate MP 324 in S. nigrum acc. 984750019. This gene, conferring resistance to P. infestans, may be useful for the transformation of potato cultivars susceptible to late blight.     

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.     

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     

粘虫抗甲氨基阿维菌素苯甲酸盐种群的交互抗性与生化抗性机制

为指导甲氨基阿维菌素苯甲酸盐（下称甲维盐）在粘虫Mythimna separate Walker防治上的合理使用,测定了粘虫抗甲维盐种群对5种常用杀虫剂的交互抗性及其生化抗性机制。结果表明:粘虫抗甲维盐种群对阿维菌素（抗性倍数RR₅₀=21.80）、毒死蜱（RR₅₀=17.68）和灭多威（RR₅₀=10.85）均具有中等水平的交互抗性,与辛硫磷（RR₅₀=6.00）和氟氯氰菊酯（RR₅₀=5.65）之间交互抗性水平较低。酶抑制剂胡椒基丁醚（PBO）、马来酸二乙酯（DEM）、三丁基三硫磷酸酯（DEF）和磷酸三苯酯（TPP）在粘虫敏感种群和抗性种群生物测定中对甲维盐毒力均有显著的增效作用。粘虫抗甲维盐种群细胞色素P450和b₅含量及O-脱甲基酶、谷胱甘肽S-转移酶和羧酸酯酶活性均显著高于敏感种群,分别为敏感种群的3.23、3.65、3.63、1.64和2.66倍。研究表明,体内解毒代谢酶活性提高可能是粘虫对甲维盐产生抗性的重要原因。     

psbA mutation (Asn266 to Thr) in Senecio vulgaris L. confers resistance to several PS II-inhibiting herbicides

DNA sequence analysis of the psbA gene encoding the D1 protein of photosystem II (PS II), the target site of PS II-inhibiting herbicides, identified a point mutation (Asn266 to Thr) in a bromoxynil-resistant Senecio vulgaris L. population collected from peppermint fields in Oregon. Although this mutation has been previously reported in Synechocystis, this is the first report of this particular point mutation in a higher plant exhibiting resistance to PS II-inhibiting herbicides. The resistant population displayed high-level resistance to bromoxynil and terbacil (R/S ratio 10.1 and 9.3, respectively) and low-level resistance to metribuzin and hexazinone (R/S ratio 4.2 and 2.6, respectively) when compared with the susceptible population. However, the population was not resistant to the triazine herbicides atrazine and simazine or to the urea herbicide diuron. A chlorophyll fluorescence assay confirmed the resistance levels and patterns of cross-resistance of the whole-plant studies. The resistant S. vulgaris plants produced fewer seeds. Differences in cross-resistance patterns to PS II-inhibiting herbicides and the difference in fitness cost could be exploited in a weed management program.     

中国北方部分地区麦田荠菜对苯磺隆的抗性水平

为明确北方地区冬小麦田荠菜对苯磺隆的抗性水平,运用培养皿法和温室盆栽法分别测定了山东、山西、河南、河北、陕西5省13个地区采集点麦田潜在抗药性生物型对苯磺隆的抗性水平,并分别测定了驻马店梁祝镇采集点荠菜潜在抗药性生物型和敏感生物型乙酰乳酸合成酶(ALS)对苯磺隆的敏感性。培养皿法测定结果表明:驻马店梁祝镇采集点荠菜抗药性生物型对苯磺隆的抗性水平最高,抗性倍数为6.17倍,其他采集点荠菜抗性倍数在0.94～2.04倍之间,仍处于较为敏感状态。温室盆栽法测定结果表明:驻马店梁祝镇采集点荠菜抗性倍数仍为最高,达到233倍, 其他地区采集点荠菜抗性倍数在1.23～3.73倍之间,尚未产生明显的抗药性。离体条件下,苯磺隆对荠菜抗药性和敏感生物型ALS的抑制中浓度(IC50)分别为0.664 μmol/L和0.053 3 μmol/L,抗药性生物型的抗性倍数达12.5倍。结果表明,驻马店梁祝镇采集点荠菜已对苯磺隆产生了较高水平的抗药性,而其体内ALS敏感性降低可能是抗药性产生的原因之一。