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.     

谷蠹和米象对磷化氢抗性遗传的研究

本文就谷蠹Rhyzopertha dominica 和米象Sitophilus oryzae对磷化氢的抗性遗传进行了研究,分别对两个种的实验室敏感品系和粮仓现场采集的抗性品系作为亲本进行杂交。同时测定了各自的亲本及其F₁杂种、F₁对抗性亲本回交和F2混交后代的剂量-死亡率反应曲线,并对它们的结果进行了遗传分析。结果指出,谷蠹和米象的F₁杂种对磷化氢的抗性遗传都为不完全隐性,各自的显性度(D)分别是-0.768和-0.348。同时F₁,回交和F₂混交的观察值和计算值之间的X²分析也表明,抗性表现为一个以上的常染色体因子遗传,但是主要是受隐性因子所控制。     

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.     

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.     

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.     

Inheritance of diflubenzuron resistance and monooxygenase activities in a laboratory-selected strain of Lucilia cuprina (Diptera: Calliphoridae).

Inheritance of the high-level diflubenzuron resistance shown by a laboratory-selected strain of Lucilia cuprina (Wiedemann) was examined in matings with a susceptible reference strain. Progeny of reciprocal crosses between resistant females and susceptible males showed higher LC50 values than the alternate reciprocal cross, indicating some maternal influence on inheritance of resistance. Resistance was inherited in a codominant (S male x R female) or incompletely recessive (R male x S female) manner. Monooxygenase activities (aldrin epoxidation) of the F1 generations were also intermediate between the levels shown by the parental lines, however, inheritance of enzyme activities showed greater degrees of dominance than for resistance levels. There was also some maternal influence on inheritance of monooxygenase activities. Backcrosses of F1 generations to both susceptible and resistant parents did not fit the expected patterns for a major sex-linked resistance locus, indicating that the maternal influence on resistance inheritance was not associated with sex-linkage of a major resistance gene. The backcross data also failed to fit the model for a single major autosomal gene, suggesting that the resistance in the diflubenzuron-selected strain is polygenic, involving mechanisms additional to monooxygenases.     

Genetic basis of resistances to chlorfenapyr and etoxazole in the two-spotted spider mite (Acari: Tetranychidae)

We studied the genetic basis of resistance to two new acaricides, chlorfenapyr and etoxazole, which have different chemical structures and modes of action in the two-spotted spider mite, Tetranychus urticae Koch. The resistance ratios calculated from the LC50s of resistant and susceptible strains were 483 for chlorfenapyr and >100,000 for etoxazole. Mortality caused by the two acaricides in F1 progeny from reciprocal crosses between the resistant and susceptible strains indicated that the modes of inheritance of resistance to chlorfenapyr and etoxazole were completely dominant and completely recessive, respectively. Mortality in F2 progeny indicated that for both acaricides, the resistance was under monogenic control. Repeated backcross experiments indicated a linkage relationship among the two acaricide resistances and malate dehydrogenase, although phosphoglucoisomerase was not linked with them. The recombination ratio between the resistances was 14.8%. From this result, we suggest that heavy spraying of the two acaricides will lead to apparent cross-resistance as a consequence of crossing over; the two resistance genes are so close to each other that it would be difficult to segregate them once they came together on the same chromosome.     

Inheritance of Cry1F resistance in laboratory-selected European corn borer and its survival on transgenic corn expressing the Cry1F toxin

A major assumption of the high-dose/refuge strategy proposed for insect resistance management strategies for transgenic crop plants that express toxins from Bacillus thuringiensis is that resistance traits that evolve in pest species will be recessive. The inheritance of Cry1F resistance and larval survival on commercially available Cry1F corn hybrids were determined in a laboratory-selected strain of European corn borer, Ostrinia nubilalis (Hübner), displaying more than 3000-fold resistance to Cry1F. Concentration-response bioassays of reciprocal parental crosses indicated that the resistance is autosomal and recessive. Bioassays of the backcross of the F1 generation with the selected strain were consistent with the hypothesis that a single locus, or a set of tightly linked loci, is responsible for the resistance. Greenhouse experiments with Cry1F-expressing corn hybrids indicated that some resistant larvae survived the high dose of toxin delivered by Cry1F-expressing plants although F1 progeny of susceptible by resistant crosses had fitness close to zero. These results provide the first direct evidence that the high dose/refuge strategy currently in place to manage resistance in Cry1F-expressing corn is appropriate.     

西花蓟马对多杀菌素的抗性汰选和遗传方式

在室内进行了西花蓟马Frankliniella occidentalis(Pergande)种群对多杀菌素的抗性筛选和抗性遗传方式分析。经过2年多的汰选,抗性水平相比较初始种群提高了30倍,与同时测定的敏感品系相比抗性达到80.8倍。抗性遗传方式分析结果表明,正、反交后代显性度分别为0.51和0.43,二者差异不显著,说明西花蓟马对多杀菌素的抗性为常染色体、不完全显性遗传;剂量对数死亡机率值曲线分析结果显示回交后代在死亡率50%处,自交后代在死亡率25%和75%处未出现明显平坡,回交和自交后代实测值卡方检验进一步证实抗性为多基因控制。     

Inheritance of resistance to flumethrin in the Mexican Aldama strain of the cattle tick Boophilus microplus (Acari: Ixodidae)

The objective of this study was to evaluate the inheritance mode of resistance to flumethrin in the Mexican Aldama Boophilus microplus strain. Two Mexican strains were used, the Chiapas susceptible (SS), and the Aldama flumethrin-resistant from Tamaulipas. Six steers weighing ca. 250 kg were randomly assigned for each of six crosses: the susceptible (SS), resistant (RR), and the F1 (RS, SR) reciprocal crosses and F2 (RS x RS and SR x SR). The reciprocal crosses were made to evaluate maternal and sex linkage effects. Bioassays tested resistant and susceptible larvae along with their hybrid F1 and F2 progeny against a series of concentrations of flumethrin (0, 0.0075, 0.00150, 0.00300, 0.00600 and 0.01200 microg/g). To test the single-gene hypothesis of resistance, a nonparametric line-cross test proposed by Collins was used. The bioassay data were subjected to probit analysis and the resistance factor and effective dominance obtained. Results of this study indicated that inheritance for flumethrin resistance in the Aldama strain was autosomal and controlled for more than one gene. The F1 and F2 larvae had similar lower resistant factor (RF 2.8-4.5) while the resistant Aldama strain was 21-fold higher (RF 81.8) than the mean of the F1 and F2. The extent of flumethrin resistance in the Aldama B. microplus strain depended upon the concentration of the pesticide used. Resistance was almost dominant at the lowest dose while almost completely recessive at the highest dose. Maternal effects were shown for egg-mass. These results shown here indicate more than one gene basis of flumethrin resistance in B. microplus ticks are present. Therefore it is necessary to locate and understand the major loci for elucidate the mechanism of resistance and improve the ability to track and delay the evolution of resistance.     

Inheritance of dicrotophos resistance in greenhouse whitefly

We studied inheritance of resistance to dicrotophos in greenhouse whitefly,Trialeurodes vaporariorum Westwood (Homoptera, Aleyrodidae). Compared with females from a field-collected susceptible strains (S), females from a resistant strain (R) ofT. vaporariorum derived from heavily treated cotton fields had a 28-fold greater LC₅₀ to dicrotophos in laboratory bioassays. Concentration-mortality lines obtained from female progeny of reciprocal F₁ crosses (R_♀ XS_♂ and S_♀ XR_♂) were similar, suggesting that inheritance of dicrotophos resistance was autosomal and not influenced by maternal effects. Responses of F₁ female progeny were similar to those of the parental S strain, indicating that the resistance was partially recessive (degree of dominance, D, was −0.61). Mortality observed in female progeny obtained from a backcross (F_1♀ XR_♂) corresponded more closely to expectations derived from polygenic models than to expectations from a monogenic model. The estimated number of effective factors (sensu Lande, 1981) contributing equally to resistance was three.     

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 F₁ reciprocal crosses and backcrosses between F₁ 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 F₁ crosses were identical, indicating that the resistant trait was autosomal. The 50% lethal concentration for the F₁ larvae was slightly higher than that for P_S, suggesting that resistance is partially recessive. The responses of both backcross progeny (F₁ × P_R, F₁ × 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 F₁ × P_R backcross but decreased the correspondence with the F₁ × 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.     

Genetics and fitness costs of cyromazine resistance in the house fly (Diptera: Muscidae)

The genetic basis of cyromazine resistance was investigated in the house fly, Musca domestica L. The ED-R strain, which was collected in Mississippi and selected further in the laboratory, was 116.5-fold resistant compared with the laboratory susceptible strain, OR-S. The SEL strain, which was created by crossing ED-R with OR-S followed by three cycles of reselection and backcrossing to OR-S, was 84.7-fold resistant relative to the susceptible strain. Mortality data from reciprocal crosses of resistant and susceptible flies indicated that resistance was autosomal and not influenced by maternal effects. The relative position of probit lines from the parental strains and reciprocal crosses showed that resistance was expressed as an incompletely dominant trait with D = 0.30 and 0.32 for ED-R and SEL, respectively. To determine the number of genes involved, models of one, two, three, four, and five loci were used to compare observed and expected mortality of F1ED-R x susceptible backcross. Resistance was best described by a polygenic model of three loci when equal and additive effects of loci were assumed. Another approach, which was based on phenotypic variances, showed that nE, or the minimum number of freely segregating genetic factors for ED-R, equaled 3.07. ED-R showed greater reductions in fitness compared with SEL independent of the presence or absence of sublethal concentrations of cyromazine. These data suggested that reduced fitness was not due to deleterious pleiotropic effects of the resistance genes themselves but arose from other loci in the ED-R genotype.     

Testing Anopheles albimanus for genetic linkage of insecticide resistance genes by combining insecticide bioassay and biochemical methods

A microtitre-plate assay which distinguishes propoxur-resistant from susceptibles Anopheles albimanus Weidemann was used to test for linkage between the genes for propoxur- and dieldrin-resistance. The adult progeny of a backcross between a doubly-resistant colony and a fully susceptible colony were exposed in conventional test kits to the standard discriminating dose of dieldrin, and kept in the insectary overnight. Both live and dead insects were then assayed individually for propoxur-resistance. The results showed that heterozygotes for propoxur-resistance could be reliably distinguished from susceptibles whether or not they had been killed up to 24 h previously by dieldrin treatment. In this way all the backcross progeny could be scored at both resistance loci, and all four genotypic classes identified. Resistant and susceptible alleles at the two loci were inherited independently, demonstrating the absence of linkage. The usual method of testing for linkage between resistance genes is inefficient and open to bias, because insects have to be exposed to each insecticide in turn, and only half of them can be scored at both loci. The method shown here avoids these drawbacks.     

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.     

Levamisole resistance in Trichostrongylus colubriformis: a sex-linked recessive character

Reciprocal crosses between susceptible and levamisole resistant strains of Trichostrongylus colubriformis produced F1 offspring consistent with resistance being inherited as a sex-linked recessive character. The resistance status of the offspring of the backcrosses of the F1 to both parental strains supported this hypothesis. The results are consistent with resistance being controlled by a single gene, or a tightly linked group of genes, but indicate that other autosomal loci have minor effects. The results contrast with the reported observations that resistance to the benzimidazole anthelmintics is polygenic and autosomal. The results are discussed relative to a general evolutionary model for anthelmintic resistance which predicts that selection from the upper extreme of an anthelmintic tolerance distribution results in polygenicity.     

Selection of dieldrin-resistant strains of Lucilia cuprina (Diptera: Calliphoridae) after ethyl methanesulfonate mutagenesis of a susceptible strain.

After ethyl methanesulfonate (EMS) mutagenesis of a susceptible strain (SWT), selective screening of Lucilia cuprina (Wiedemann) resulted in four strains that were resistant to the insecticide dieldrin. Concentrations used for selection were greater than LC99 of susceptible phenotypes. No resistant variants were screened from the standard laboratory strain (SWT) not treated with EMS. The resistance phenotypes of the four resistant strains were similar to each other and to that of a field-selected resistant strain. The genetic basis of resistance is monogenic in all strains and the data are consistent with the same locus, Rdl, determining resistance status in each strain. The Rdl locus maps to chromosome V, approximately 3.5 map units distal to the Sut locus. Dieldrin resistance may be caused by less effective blocking of insect neuronal GABA receptors by the chemical in resistant strains. The data indicate that the evolution of resistance to an insecticide in the field may be constrained by a limited number of genetical and biochemical options if a monogenic response is selected for and that the spontaneous mutation rate to the Rdl allele is less than 1 in 10(6) in the laboratory.     

Five independent loci each control monogenic resistance to gummy stem blight in melon (<Emphasis Type="Italic">Cucumis melo</Emphasis> L.)

Inheritance and segregation analysis demonstrated that five independent genes in melon confer monogenic resistance to foliar infection by the fungal pathogen Didymella bryoniae, resulting in the disease known as gummy stem blight (GSB). In this study, two new monogenic sources of GSB resistance were characterized. Resistance in Cucumis melo PI 482398 was monogenic dominant based on segregation analysis of F₁, F₂ and backcross populations, while resistance in C. melo PI 482399 showed monogenic recessive inheritance. Four accessions, PI 482398, PI 157082, PI 511890, and PI 140471, each previously known to carry monogenic dominant resistance to GSB, were intercrossed to determine genetic relationships among these resistance sources. Recovery of susceptible individuals in F₂ populations confirmed that these accessions possess different resistance genes. Resistance loci were designated Gsb-1 (formerly Mc, monogenic dominant resistance from PI 140471), Gsb-2 (monogenic dominant resistance from PI 157082), Gsb-3 (monogenic dominant resistance from PI 511890), Gsb-4 (monogenic dominant resistance from PI 482398) and gsb-5 (monogenic recessive resistance from PI 482399).Communicated by J. Dvorak     

Genetic control of resistance to Coccidioides immitis: a single gene that is expressed in spleen cells determines resistance

We have previously reported that inbred mice vary widely in their resistance to Coccidioides immitis peritonitis. To investigate the number of genes controlling resistance, (susceptible X resistant)F1 X susceptible backcross mice were tested for resistance to infection. A 1:1 ratio of resistant:susceptible offspring was observed, which is consistent with a single dominant gene determining resistance. To find out whether this gene, which we designated Cms, is expressed in the immune and/or the inflammatory responses, radiation chimeras were constructed by transplanting spleen cells from the resistant F1 mice into the susceptible parental strain. These chimeras were consistently more resistant to infection than the susceptible parental strain. We concluded that resistance to C. immitis is determined primarily by a single gene, and that this gene is expressed by spleen cells.     

Genetic identification of distinct loci controlling mammary tumor multiplicity, latency, and aggressiveness in the rat

The rat is considered an excellent model for studying human breast cancer. Therefore, understanding the genetic basis of susceptibility to mammary cancer in this species is of great interest. Previous studies based on crosses involving the susceptible strain WF (crossed with the resistant strains COP or WKY) and focusing on tumor multiplicity as the susceptibility phenotype led to the identification of several loci that control chemically induced mammary cancer. The present study was aimed to determine whether other loci can be identified by analyzing crosses derived from another susceptible strain on the one hand, and by including phenotypes other than tumor multiplicity on the other hand. A backcross was generated between the susceptible SPRD-Cu3 strain and the resistant WKY strain. Female progeny were genotyped with microsatellite markers covering all rat autosomes, treated with a single dose of DMBA, and phenotyped with respect to tumor latency, tumor multiplicity, and tumor aggressiveness. Seven loci controlling mammary tumor development were detected. Different loci control tumor multiplicity, latency, and aggressiveness. While some of these loci colocalize with loci identified in crosses involving the susceptible strain WF, new loci have been uncovered, indicating that the use of distinct susceptible and resistant strain pairs will help in establishing a comprehensive inventory of mammary cancer susceptibility loci.