西花蓟马抗辛硫磷种群的抗性机制及交互抗性

为明确西花蓟马对辛硫磷的抗性风险,研究了西花蓟马抗辛硫磷种群对其他杀虫剂的交互抗性及其对辛硫磷的抗性机制.交互抗性测定结果表明,西花蓟马抗辛硫磷种群对辛硫磷与毒死蜱、高效氯氟氰菊酯和灭多威存在中等水平的交互抗性,对溴虫腈、吡虫啉、甲维盐和多杀菌素存在低水平交互抗性,对啶虫脒和阿维菌素不存在交互抗性.酶抑制剂与辛硫磷的增效剂测定结果表明,胡椒基丁醚(PBO)、三丁基三硫磷酸酯(DEF)和磷酸三苯酯(TPP)对西花蓟马抗辛硫磷种群(XK)、田间种群(BJ)和敏感种群(S)均起到了显著的增效作用(P＜0.05),马来酸二乙酯对西花蓟马抗辛硫磷种群和敏感种群增效作用均不显著,但对田间种群增效作用显著(P＜0.05).生化测定发现:除田间种群西花蓟马乙酰胆碱酯酶活性提高不显著外,西花蓟马抗辛硫磷种群和田间种群的细胞色素P450含量(2.79和1.48倍)、细胞色素b5含量(2.88和1.88倍)及O-脱甲基酶活性(2.60和1.68倍)、羧酸酯酶活性(2.02和1.61倍)和乙酰胆碱酯酶活性(3.10倍)均显著高于敏感种群(P＜0.05);谷胱甘肽-S-转移酶酶活性也有一定程度提高(1.11和1.20倍),但不显著(P＞0.05).表明其体内解毒代谢酶和靶标酶活性提高是西花蓟马对辛硫磷产生抗性的重要原因.     

西花蓟马抗噻虫胺种群对杀虫剂的交互抗性及机制

噻虫胺是具有内吸和触杀等多种作用方式的新烟碱类杀虫剂,常用于防治入侵害虫西花蓟马。为明确抗性风险,本文研究了西花蓟马抗噻虫胺种群对多种杀虫剂的交互抗性及其机制。经过45代筛选,西花蓟马对噻虫胺产生了高水平抗性(56.8倍)。生物测定结果表明: 西花蓟马高抗噻虫胺种群与噻虫嗪、吡虫啉、毒死蜱、三氟氯氰菊酯、甲维盐存在中等水平交互抗性(18.6>RR₅₀>11.3),对辛硫磷及灭多威具有低水平交互抗性,与溴虫腈和多杀菌素不存在交互抗性。胡椒基丁醚(PBO)与磷酸三苯酯(TPP)对杀灭西花蓟马抗噻虫胺种群(CL)、云南田间种群(YN)和敏感种群(S)均有显著增效作用。西花蓟马抗噻虫胺种群细胞色素P₄₅₀含量(3.6倍)、细胞色素b₅含量(2.9倍)及O-脱甲基酶活性(4.9倍)和羧酸酯酶活性(2.5倍)均显著高于敏感种群,表明多功能氧化酶及羧酸酯酶活性增强是西花蓟马对噻虫胺产生抗性的重要机制。     

北京和云南地区西花蓟马对多杀菌素类药剂产生抗药性

【目的】了解我国西花蓟马Frankliniella occidentalis(Pergande)对多杀菌素等药剂的抗药性现状,为西花蓟马的有效防治提供参考。【方法】2011—2015年,采用叶管药膜法对北京和云南地区西花蓟马进行了抗药性监测。【结果】与室内敏感品系相比,北京地区西花蓟马田间种群对多杀菌素的抗性倍数达到80~150倍,对乙基多杀菌素抗性倍数高达7 730倍,对乙基多杀菌素的LC50值5年间最高增加了258倍,对甲维盐和噻虫嗪具有中等水平抗性,对阿维菌素和虫螨腈处于敏感或低水平抗性;昆明地区西花蓟马对乙基多杀菌素的抗性水平达到305倍的极高抗水平,对其它药剂相对敏感或处于低水平抗性。【结论】北京和云南地区西花蓟马对多杀菌素类药剂已经产生高水平抗药性,应密切关注抗性发展动态,同时进一步研究其抗性机制。     

北京地区西花蓟马田间种群的抗药性监测

采用叶管药膜法在室内测定了2009—2010年北京海淀地区和昌平地区西花蓟马Frankliniella occidentalis(Pergande)田间种群对12种杀虫剂敏感性的年度变化。结果表明,北京昌平和海淀地区的西花蓟马对多数的药剂仍处于敏感状态,但对氯氟氰菊酯已产生近40倍的抗性,昌平种群对多杀菌素具有产生低水平抗性的趋势(抗性倍数为4倍)。推荐药剂包括多杀菌素、阿维菌素、甲氨基阿维菌素苯甲酸盐(甲维盐)、毒死蜱和溴虫腈,应注意与其它药剂的轮换使用,灭多威对西花蓟马的毒力水平最低,不推荐使用。     

西花蓟马对吡虫啉、辛硫磷和甲维盐的抗性风险和抗性稳定性

为有效控制西花蓟马的危害,采用吡虫啉、辛硫磷和甲维盐药液浸泡芸豆法,分别对西花蓟马敏感种群成虫进行抗性选育,获得抗性种群,应用抗性现实遗传力分析抗性遗传和抗性风险.结果表明:经过32代、32代和24代抗性选育,西花蓟马对吡虫啉、辛硫磷和甲维盐的抗性分别达到13.8、29.4和39.0倍.西花蓟马对吡虫啉、辛硫磷和甲维盐的现实抗性遗传力分别为0.112、0.166和0.259,西花蓟马对甲维盐的抗性上升速度最快,辛硫磷次之,吡虫啉最低.经过药剂筛选后,西花蓟马若虫与成虫对杀虫剂的敏感性差异较敏感种群显著缩小.停止用药剂筛选后继续饲养12代,西花蓟马对吡虫啉、辛硫磷和甲维盐的抗性水平都有一定程度下降,但都没有恢复到敏感性水平.西花蓟马对吡虫啉、辛硫磷和甲维盐具有较高水平抗性的风险,其中对吡虫啉的抗性发展速度相对较慢,且下降速度较快,因此选用吡虫啉防治西花蓟马更合适.     

番茄斑萎病毒对多杀菌素抗性西花蓟马发育繁殖和药剂敏感性的影响

【目的】西花蓟马Frankliniella occidentalis (Pergande)是重要的入侵害虫,是番茄斑萎病毒（TSWV）最有效的传播媒介,TSWV对西花蓟马的生长发育有一定的影响。多杀菌素是防治西花蓟马最有效的药剂之一,但已有田间西花蓟马对多杀菌素产生抗药性的报道。TSWV对抗性西花蓟马是否也有影响及程度如何尚不清楚。本研究通过对此问题进行深入研究,以期为进一步了解TSWV对西花蓟马的影响提供依据。【方法】应用特定年龄-龄期及两性生命表的方法,研究用番茄斑萎病毒处理和未处理的多杀菌素抗性和敏感西花蓟马种群的生物学特性;用叶管药膜法测定不同处理种群对3种药剂（多杀菌素、甲氨基阿维菌素苯甲酸盐和虫螨腈）的敏感性变化。【结果】对于抗性品系,TSWV处理后西花蓟马的发育历期缩短,雌成虫寿命和产卵量略高,但与对照组差异不显著(P＞0.05),内禀增长率（r）和净生殖率（R₀）分别为0.0433 d^-1和2.210,显著高于对照组（分别为0.0356 d^-1和1.972）（P ≤ 0.001）。对于敏感品系,TSWV处理后西花蓟马的发育历期缩短,雌雄成虫寿命均显著延长（P ≤ 0.001）,产卵量也略有提高,R₀为4.125,显著高于对照组（3.979）（P ≤ 0.001）。TSWV处理后敏感和抗性西花蓟马对多杀菌素的敏感性没有发生明显变化,对甲氨基阿维菌素苯甲酸盐和虫螨腈的敏感性显著降低。【结论】番茄斑萎病毒对多杀菌素敏感和抗性西花蓟马均有直接有利影响,病毒处理的西花蓟马发育历期缩短,繁殖能力增强,成虫寿命延长,对药剂的敏感性降低。     

棉铃虫对Bt杀虫剂的抗性遗传方式

随着转基因棉花种植面积的日益增加,棉铃虫Helicoverpa armigera（Hübner)对Bt的抗性已经成为一个不容忽视的问题。发展转多价基因作物是当前缓解害虫对Bt抗性的最有效措施。本研究以经室内多年筛选的、抗性倍数达2 000多倍的Bt杀虫剂（含多种蛋白）抗性品系为材料,通过生物测定和不同的杂交试验,测定棉铃虫对Bt杀虫剂的抗性遗传方式,以期为Bt生物农药的抗性治理提供一定的依据,同时为制定棉铃虫对转多基因作物的抗性治理策略提供一定的参考。对敏感亲本和抗性亲本杂交产生的F1代的研究结果表明,杂交品系的抗性倍数分别为22.2倍和24.6倍;抗性显性度D值均小于0,分别为-0.20和-0.17,抗性为常染色体不完全隐性遗传。对4种回交后代和2种自交后代F2的研究结果表明,实际死亡率与期望死亡率差异较大,说明抗性是由单基因多个位点或多基因控制。     

褐飞虱对马拉硫磷的抗性遗传和交互抗性研究

毒力测定显示,抗马拉硫磷品对杀螟松、二嗪磷、异丙威和仲丁威都有明显的交互抗性产生,但对醚菊酯和吡虫啉没有表现出显的交互抗性。抗性遗传研究显示,正交和反交后代F1和F1'的显性值D分别为0.4014和0.3780,说明抗性主效基因是不完全显性的。通过自交后代F2和回交后代BC的LD-p线观察及与期望曲线比较,证明抗性遗传由两个或两个以上的基因控制。     

西花蓟马对烯啶虫胺、噻虫胺和噻虫嗪的抗性风险和抗性稳定性

为明确使用新烟碱类杀虫剂烯啶虫胺、噻虫胺和噻虫嗪防治入侵害虫西花蓟马的抗性风险及抗性稳定性,本研究采用芸豆浸药法对西花蓟马敏感种群初羽化雌成虫进行连续筛选获得抗性种群,根据抗性现实遗传力计算公式分析西花蓟马对上述3种杀虫剂的抗性风险,预测其抗性发展速度,并测定抗性稳定性。结果表明: 经过30代抗性筛选,西花蓟马对烯啶虫胺、噻虫胺和噻虫嗪均达到高水平抗性(44.7、45.5和32.7倍)。西花蓟马对噻虫胺、烯啶虫胺和噻虫嗪的抗性发展速度依次降低,抗性现实遗传力分别为0.1503、0.1336和0.1258。对抗性种群在无选择压力下继续饲养10代,西花蓟马对烯啶虫胺、噻虫胺和噻虫嗪的抗性水平均出现一定程度的下降,但均未能恢复到敏感性水平。抗性选育后,西花蓟马若虫与成虫对杀虫剂的敏感性差异显著缩小,西花蓟马敏感种群及抗性种群若虫对上述3种杀虫剂的敏感性显著高于成虫。西花蓟马对烯啶虫胺、噻虫胺和噻虫嗪均存在高抗风险,噻虫嗪的抗性上升速度较慢且抗性稳定性最低。因此,在西花蓟马若虫期使用噻虫嗪有利于西花蓟马防治。     

西花蓟马的抗药性及其治理策略

西花蓟马Frankliniella occidentalis（Pergande）是世界性的园艺作物上的重要害虫,几乎对每种类型的杀虫剂均产生了抗药性,包括有机磷、氨基甲酸酯、拟除虫菊酯类杀虫剂和多杀菌素等。本文对国外西花蓟马的抗药性发展现状和抗性机制进行了总结,并提出了抗性治理策略,即科学合理使用杀虫剂,结合栽培防治、物理防治、生物防治和寄主植物抗性等方式降低杀虫剂对西花蓟马的选择压,从而达到抗性治理的目的。     

Inheritance of Cry1Ac resistance and associated biological traits in the cotton bollworm, Helicoverpa armigera (Lepidoptera: Noctuidae)

The analysis of reciprocal genetic crosses between resistant Helicoverpa armigera strain (BH-R) (227.9-fold) with susceptible Vadodara (VA-S) strain showed dominance (h) of 0.65-0.89 and degree of dominance (D) of 0.299-0.782 suggesting Cry1Ac resistance as a semi-dominant trait. The D and h values of F₁ hybrids of female resistant parent were higher than female susceptible parent, showing maternally enhanced dominance of Cry1Ac resistance. The progeny of F₂ crosses, backcrosses of F₁ hybrid with resistant BH-R parent did not differ significantly in respect of mortality response with resistant parent except for backcross with female BH-R and male of F₁ (BH-R × VA-S) cross, suggesting dominant inheritance of Cry1Ac resistance. Evaluation of some biological attributes showed that larval and pupal periods of progenies of reciprocal F₁ crosses, backcrosses and F₂ crosses were either at par with resistant parent or lower than susceptible parent on treated diet (0.01 μg/g). The susceptible strain performed better in terms of pupation and adult formation than the resistant strain on untreated diet. In many backcrosses and F₂ crosses, Cry1Ac resistance favored emergence of more females than males on untreated diet. The normal larval period and the body weight (normal larval growth) were the dominant traits associated with susceptible strain as contrast to longer larval period and the lower body weight (slow growth) associated with resistance trait. Further, inheritance of larval period in F₂ and backcross progeny suggested existence of a major resistant gene or a set of tightly linked loci associated with Cry1Ac sensitivity.     

Inheritance of resistance to Bt toxin crylac in a field-derived strain of pink bollworm (Lepidoptera: Gelechiidae)

Laboratory selection with Cry1Ac, the Bacillus thuringiensis (Bt) toxin in transgenic cotton, initially produced 300-fold resistance in a field-derived strain of pink bollworm, Pectinophora gossypiella (Saunders), a major cotton pest. After additional selection increased resistance to 3,100-fold, we tested the offspring of various crosses to determine the mode of inheritance of resistance to Cry1Ac. The progeny of reciprocal F1 crosses (resistant male x susceptible female and vice versa) responded alike in bioassays, indicating autosomal inheritance. Consistent with earlier findings, resistance was recessive at a high concentration of Cry1Ac. However, the dominance of resistance increased as the concentration of Cry1Ac decreased. Analysis of survival and growth of progeny from backcrosses (F1 x resistant strain) suggest that resistance was controlled primarily by one or a few major loci. The progression of resistance from 300- to 3,100-fold rules out the simplest model with one locus and two alleles. Overall the patterns observed can be explained by either a single resistance gene with three or more alleles or by more than one resistance gene. The pink bollworm resistance to Cry1Ac described here fits "mode 1" resistance, the most common type of resistance to Cry1A toxins in Lepidoptera.     

Inheritance of resistance to the Cry1Ab Bacillus thuringiensis toxin in Ostrinia nubilalis (Lepidoptera: Crambidae)

Laboratory selection with Cry1Ab, the predominant Bacillus thuringiensis (Bt) toxin in transgenic corn, Zea mays L., produced >1000-fold resistance in two laboratory strains of European corn borer, Ostrinia nubilalis (Hübner). We tested the offspring of various crosses to determine the mode of inheritance of resistance to Cry1Ab. Patterns of inheritance of resistance were similar in the two resistant strains. The progeny of reciprocal F1 crosses (resistant male x susceptible female and vice versa) responded alike in bioassays, indicating autosomal inheritance. The median lethal concentrations (LC50 values) of F1 were intermediate between the resistant and susceptible parents, indicating approximately additive inheritance. However, the dominance of resistance increased as the concentration of Cry1Ab decreased. Analysis of progeny from backcrosses (F1 x susceptible strain) suggests that resistance was controlled by more than one locus. In particular, the fit of observed to expected mortality improved as the number of putative loci increased from 1 to 10. The polygenic nature of resistance in these two laboratory strains suggests that major genes for resistance to Cry1Ab were not common in the founding populations of O. nubilalis. A low initial frequency of major genes for Cry1Ab resistance might be an important factor in delaying evolution of resistance to Bt corn in this pest.     

Stability of spinosad resistance in Frankliniella occidentalis (Pergande) under laboratory conditions

The stability of spinosad resistance in western flower thrips (WFT), Frankliniella occidentalis (Pergande), populations with differing initial frequencies of resistance was studied in laboratory conditions. The stability of resistance was assessed in bimonthly residual bioassays in five populations with initial frequencies of 100, 75, 50, 25 and 0% of resistant individuals. There were no consistent changes in susceptibility of the susceptible strain after eight months without insecticide pressure. In the resistant strain, very highly resistant to spinosad (RF50>23,000-fold), resistance was maintained up to eight months without further exposure to spinosad. In the absence of any immigration of susceptible genes into the population, resistance was stable. In the case of the population with different initial frequency of resistant thrips, spinosad resistance declined significantly two months later in the absence of selection pressure. With successive generations, these strains did not change significantly in sensitivity. Spinosad resistance in F. occidentalis declined significantly in the absence of selection pressure and the presence of susceptible WFT. These results suggest that spinosad resistance probably is unstable under field conditions, primarily due to the immigration of susceptible WFT. Factors influencing stability or reversion of spinosad resistance are discussed.     

Genetics of spinosad resistance in Frankliniella occidentalis (Thysanoptera: Thripidae)

The genetic basis of spinosad resistance was investigated in the western flower thrips, Frankliniella occidentalis (Pergande) (Thysanoptera: Thripidae). The resistant strain, selected in the laboratory for spinosad resistance from a pool of thrips populations collected in Almeria (southeastern Spain), showed a very high resistance to spinosad (356,547-fold based on LC50 values) compared with the laboratory susceptible strain. Mortality data from reciprocal crosses of resistant and susceptible thrips indicated that resistance was autosomal and not influenced by maternal effects. Analysis of probit lines from the parental strains and reciprocal crosses showed that resistance was expressed as an almost completely recessive trait. To determine the number of genes involved, a direct test of monogenic inheritance based on the backcrosses suggested that resistance to spinosad was probably controlled by one locus. Another approach, which was based on phenotypic variances, showed that nE, or the minimum number of freely segregating genetic factors for the resistant strain, equaled 0.59.     

Development and stability of insecticide resistance in the leafminer Liriomyza trifolii (Diptera: Agromyzidae) to cyromazine, abamectin, and spinosad

Three populations of the leafminer, Liriomyza trifolii (Burgess), were collected from commercial ornamental production greenhouses in the United States and tested for susceptibility to three commercial insecticides. A leaf dip bioassay of leaves containing young (1-2-d-old) larvae was used. Based on larval mortality and compared with a susceptible laboratory reference colony, the three strains varied in spectrum and level of resistance to the insecticides. CA-1, collected from Gerbera daisy, was moderately resistant to cyromazine (18.1-fold) and abamectin (22.0-fold), but highly resistant to spinosad (> 188-fold). CA-2, collected from chrysanthemums, was not resistant to abamectin, had a low level of resistance to cyromazine (8.2-fold), but was extremely resistant to spinosad (1,192-fold). GA-1, collected from chrysanthemums, had very low levels of resistance to cyromazine (5.4-fold) and spinosad (1.9-fold) but was moderately resistant to abamectin (30.6-fold). When reared in the absence of insecticide selection pressure, all three strains reverted to approximately the level of the reference strain. The CA-1 strain reverted in nine generations to cyromazine; however, the lowest levels of abamectin and spinosad resistance reverted to was 3.1-fold at F8 and 3.2 at the F10, respectively. The CA-2 strain reverted in five generations to both cyromazine and spinosad. GA-1 reverted in five generations to abamectin. Based on the results, resistance to these three insecticides was unstable. Additionally, there was no cross-resistance among these three insecticides.     

Field resistance of codling moth against Cydia pomonella granulovirus (CpGV) is autosomal and incompletely dominant inherited

The current appearance of local codling moth populations with resistance to Cydia pomonella granulovirus (CpGV) is an impediment to continuous CpGV application. Therefore, crossing experiments have been performed in order to gain information about the inheritance of resistance. Evidence is presented that the observed field resistance is stably inherited even under non-selective conditions in the laboratory. Offspring of reciprocal F(1) crosses between a susceptible ('S') and a resistant ('R') strain and backcrosses between F(1) and S were bioassayed at different CpGV concentrations. The resistant strain showed 100 times lower susceptibility in 7-day bioassays. The responses of the reciprocal crosses (male S x female R and female S x male R) did not differ significantly, indicating that resistance is autosomally inherited. The median lethal concentration for the F(1) progeny was intermediate between those of its parental strains. Mortality data obtained from the backcrosses suggested that inheritance of resistance is due to a non-additive, polygenic trait.     

Inheritance of resistance to Bacillus thuringiensis subsp. kurstaki in Trichoplusia ni

The genetic inheritance of resistance to a commercial formulation of Bacillus thuringiensis subsp. kurstaki was examined in a Trichoplusia ni colony initiated from a resistant population present in a commercial vegetable greenhouse in British Columbia, Canada. Progeny of F(1) reciprocal crosses and backcrosses between F(1) larvae and resistant (P(R)) and susceptible (P(S)) populations were assayed at different B. thuringiensis subsp. kurstaki concentrations. The responses of progeny of reciprocal F(1) crosses were identical, indicating that the resistant trait was autosomal. The 50% lethal concentration for the F(1) larvae was slightly higher than that for P(S), suggesting that resistance is partially recessive. The responses of both backcross progeny (F(1) x P(R), F(1) x P(S)) did not correspond to predictions from a single-locus model. The inclusion of a nonhomozygous resistant parental line in the monogenic model significantly increased the correspondence between the expected and observed results for the F(1) x P(R) backcross but decreased the correspondence with the F(1) x P(S) backcross results. This finding suggests that resistance to B. thuringiensis subsp. kurstaki in this T. ni population is due to more than one gene.     

Monitoring and characterization of diamondback moth (Lepidoptera: Plutellidae) resistance to spinosad

Fourteen populations of the diamondback moth, Plutella xylostella (L.), were collected from fields of crucifer vegetables in the United States, Mexico, and Thailand in 1999 and 2000 for susceptibility tests with spinosad. Most populations were susceptible to spinosad and similar to earlier baseline values, but populations from Thailand and Hawaii showed high levels of tolerance. A statewide survey in Hawaii in 2000 and 2001 indicated resistance problems on several islands. One colony collected in October 2000 from Pearl City, HI, was subjected to further selection pressure, using spinosad in the laboratory, and then was used as the resistant strain (Pearl-Sel) for other tests. Spray tests using the recommended field rates of spinosad on potted broccoli plants in the greenhouse confirmed that field control failures due to resistance were possible in the areas of these collections. Analysis of probit lines from F1 reciprocal crosses between the Pearl-Sel and S strain indicated that resistance to spinosad was inherited autosomally and was incompletely recessive. A direct test of monogenic inheritance based on the F1 x Pearl-Sel backcrosses suggested that resistance to spinosad was probably controlled by one locus. The synergists S,S,S-tributyl phosphorotrithioate and piperonyl butoxide did not enhance the toxicity of spinosad to the resistant colony, indicating metabolic mediated detoxification was probably not responsible for the spinosad resistance. Two field colonies in Hawaii that were resistant to spinosad were not cross-resistant to emamectin benzoate or indoxacarb. Resistance developed in Hawaii due to the continuous cultivation of crucifers in which as many as 50 applications of spinosad per year may have been made to a common population of P. xylostella in sequential plantings, although each grower might have used the labeled restrictions for resistance management. Resistance management strategies will need to address such cropping and pest management practices.     

Genetic analysis of resistance to azinphosmethyl in the pear psylla Cacopsylla pyri

Laboratory selection with azinphosmethyl had little effect on the chemical resistance in Cacopsylla pyri strains, in comparison to the original wild populations. The resistance ratio relative to a susceptible strain varied from 10- to 40-fold depending on the generation studied. Crosses between two resistant strains and the susceptible strain show resistance to be autosomally inherited and semi-dominant in expression. Backcrosses between F1 and the susceptible strain were unable to distinguish unabigously between monogenic and polygenic inheritance. In the majority of experiments, however, the overall dose-response relationship for backcross progeny was consistent with a single gene hypothesis. Additional bioassays showed azinphosmethyl-resistant strain to cross-resistant monocrotophos and phosmet, but not carbamates, pyrethroids, amitraz or the organophosphates chlorpyrifos and mevinphos.