Mode of inheritance and stability of resistance to Bacillus thuringiensis var kurstaki in a diamondback moth (Plutella xylostella) population from Malaysia

Genetic inheritance of resistance to Bacillus thuringiensis var kurstaki (BTK) was examined in a diamondback moth (Plutella xylostella) population collected from the Melaka region of Malaysia. A BTK‐selected sub‐population (BTK‐SEL) which was more than 100‐fold resistant to BTK compared with a susceptible (ROTH) population of P xylostella was used with standard reciprocal crosses and back‐crosses between ROTH and BTK‐SEL. Logit regression analysis of F ₁ reciprocal crosses indicated that BTK resistance was inherited as an incompletely recessive autosomal trait and controlled by a single locus. In contrast, other studies have shown that resistance to Cry1Ac is inherited as an incompletely dominant autosomal trait in a Cry1Ac‐selected sub‐population of the same Melaka population. The frequency of the allele responsible for resistance decreased without exposure to insecticide in the laboratory. © 2000 Society of Chemical Industry     

Genetics of host-pathogen interactions in the <Emphasis Type="Italic">Pyrenophora teres</Emphasis> f. <Emphasis Type="Italic">teres</Emphasis> (net form) – barley (<Emphasis Type="Italic">Hordeum vulgare)</Emphasis> pathosystem

The genetics of host-pathogen interactions in the Hordeum vulgare – P. teres f. teres pathosystem was studied in twelve resistant barley accessions, i.e. CI 9825, CI 9819, Diamond, CI 4922, CI 5401, Harbin, c-8755, c-21849, c-8721 c-23874, c-19979, c-15811. F₂ analyses of crosses with susceptible genotypes employing various isolates (from Europe, USA, Canada, and Australia) revealed that resistance is mostly isolate-specific and controlled by one or two genes. Segregation in ascospore progeny from two crosses between isolates of different origin revealed that avirulence in P. teres is also determined by one or two genes. An epistatic effect of suppressor genes on avirulence genes is proposed for the genetics of virulence to Diamond, Harbin, CI 5401 and c-8721 in the fungal crosses D (181-6 × A80) and F (H-22 × 92-178/9). Segregation in F₂ of crosses of three new sources of resistance (c-23874, c-19979, c-15811) to the susceptible cv. Pirkka was studied in laboratory and greenhouse tests by using seven P. teres isolates, i.e. 181-6, d8-3, d8-4, d9-1, d9-4, F4 and F74. In addition, virulence to these barley accessions of ascospore progeny from crosses of the same isolates was studied. Based on these studies it was concluded that depending on the isolate used, resistance of c-23874 is determined at least by two genes and in c-19979 and c-15811 by three genes. The results of this parallel analyses of genetics of resistance and genetics of virulence allows the postulation of a gene–for–gene interaction in the P. teres – H. vulgare pathosystem.     

Inheritance of resistance to lindane in a laboratory-selected strain of Tribolium castaneum (Herbst)

Studies on the inheritance of resistance to lindane in a laboratory-selected strain of Tribolium castaneum, by making crosses between the resistant and a susceptible strain, showed that resistance in this strain is controlled by an autosomally inherited single gene which is incompletely dominant.     

Characterization of field‐evolved resistance to Bacillus thuringiensis‐derived Cry1F δ‐endotoxin in Spodoptera frugiperda populations from Argentina

BACKGROUND

Transgenic maize (Zea mays L.) event TC1507 (Herculex^® I insect protection), expressing Cry1F δ‐endotoxin derived from Bacillus thuringiensis var. aizawai, was commercialized in 2003 in the Americas. Spodoptera frugiperda (J.E. Smith) (Lepidoptera: Noctuidae) susceptibility to Cry1F was monitored annually across several regions in Argentina using diagnostic concentration bioassays. Reduced performance of TC1507 maize against S. frugiperda was reported in 2013. A resistant population was established in the laboratory and the dominance of Cry1F resistance was characterized.

RESULTS

During 2012–2015, high‐survivorship of several populations was observed in the resistance monitoring program. Reciprocal crosses of a Cry1F‐resistant population with a Cry1F‐susceptible population were evaluated to calculate effective dominance (D_ML) based on mortality levels observed at 100 µg/ml Cry1F. Two additional dominance levels (D_LC and D_EC) were calculated using lethal (LC₅₀) or effective concentration (EC₅₀) derived from concentration–response bioassays. Estimates indicated that Cry1F resistance in S. frugiperda in Argentina was either highly recessive (D_ML = 0.005) or incompletely recessive (D_LC < 0.26 and D_EC < 0.19).

CONCLUSION

This study is the first documented confirmation and characterization of S. frugiperda Cry1F field‐evolved resistance in Argentina. The resistance to Cry1F in S. frugiperda populations collected in Argentina, is autosomal and incompletely recessive similar to the resistance reported in Brazil. © 2017 The Authors. Pest Management Science published by John Wiley © Sons Ltd on behalf of Society of Chemical Industry.     

An international campaign coordinated by EPPO to control Colorado Beetle in the Channel Islands

Collaboration between the Plant Protection Services of France and the Channel Islands has helped to keep Jersey and Guernsey free of Colorado Beetle (Leptinotarsa decemlineata) for over 60 years. The Channel Islands lie close to the coast of the Cotentin peninsula where potato fields are still infested with Colorado Beetle. Joint surveys of the coastal potato fields of Cotentin provide valuable information on beetle populations. Beetle flight records together with local weather data provide the necessary information to issue Colorado Beetle alerts to the Channel Islands during the months of May–July. High risk alerts issued by French Plant Protection colleagues are acted on and inspectors are mobilised to search beaches in Jersey and Guernsey for adult beetles. Farmers are not obliged to control Colorado Beetle in France. However, there has been an agreement negotiated in the Cotentin that farmers will treat their fields if beetles are found, with monitoring carried out by staff from a local co‐operative. This co‐operation has proved essential in the Colorado Beetle campaign.     

Field evaluation for resistance to the black rot pathogen <Emphasis Type="Italic">Xanthomonas campestris</Emphasis> pv. <Emphasis Type="Italic">campestris</Emphasis> in cabbage (<Emphasis Type="Italic">Brassica oleracea</Emphasis>)

Black rot, caused by Xanthomonas campestris pv. campestris, (Xcc), is one of the most serious diseases of crucifers world-wide. Forty-nine genotypes were evaluated for resistance under field conditions in Tanzania after artificial inoculation with Xcc race 1. Open pollinated white cabbage cultivars were generally susceptible, while Portuguese and pointed cabbages exhibited partial resistance. Some F1 white cabbage cultivars were highly susceptible, whereas others exhibited a high level of partial resistance. The most promising of the hybrid cultivars were T-689 F1, Gianty F1, No. 9690 F1, N 66 F1, and SWR-02 F1. Breeding line Badger I-16 exhibited the highest level of resistance of all genotypes. The genotypes accounted for 72.9–75.5% of the variation of the disease severity when assessed on the leaves, and 71.4% of the variation when assessed as internal black rot in heads at harvest. High correlations (equal to or above 0.7) were found between disease severities assessed on leaves three times during the growing season and also with the amount of internal black rot in heads. Leaf loss also was correlated with disease severity. The high genetic determination of the trait and the high correlations between disease assessments indicate that selection for resistance to black rot will be efficient when field screenings are carried out. Evaluation of genotypes for disease severity on leaves during the growing season combined with evaluations of head resistance in the most promising genotypes may be a simple method to select resistant cultivars.     

An evaluation of the role of oxidative enzymes in Colorado potato beetle resistance to carbamate insecticides

Carbofuran and carbaryl LD₅₀ values were determined with and without piperonyl butoxide pretreatment for a resistant (New Jersey) and two susceptible (Utah and Netherland) populations of Colorado potato beetle larvae. Similar bioassays were conducted with carbofuran for resistant (Rutgers) and susceptible (NAIDM) adult house flies. The degree of resistance development by New Jersey Colorado potato beetles (RR = 848) was greater than that of the laboratory-selected colony of Rutgers house flies (RR = 583). Comparisons of synergist difference calculations including “percentage synergism” (%S), “log percentage synergism” (L%S), and “relative percentage synergism (R%S) for the resistant (R) and the susceptible (S) populations indicated the possibility that monooxygenases and other resistance mechanisms may be involved in Colorado potato beetle resistance to these carbamates. Monooxygenase involvement in resistance of Rutgers house flies was demonstrated in vitro by a 4-fold enhancement of p-nitroanisole O-demethylation over that of NAIDM house flies. O-demethylation of p-nitroanisole could not be demonstrated for potato beetle larvae. Colorado potato beetle resistance was associated with increases in microsomal levels of NADPH-cytochrome c reductase (ca. 2-fold) and NADPH oxidation (1.2-fold). The inability to measure O-demethylation in Colorado potato beetles may have been due to the solubilization of NADPH-cytochrome c reductase during microsomal preparation. Significant differences between resistant and susceptible Colorado potato beetle larvae were not observed in the penetration of [¹⁴C]carbaryl. Excretion of the radiocarbon may have been significantly greater in the resistant New Jersey population, but some of the insecticide may have also rubbed off the cuticle. This increased capacity for excretion, combined with increased levels of monooxygenase enzymes, could account for the high resistance level of this population.     

Mode of inheritance of Indoxacarb resistance in diamondback moth, <Emphasis Type="Italic">Plutella xylostella</Emphasis> (L.) and cross resistance to different groups of pesticides

The development of insecticidal resistance in diamondback moth (DBM) Plutella xylostella has immediate implications for its management. In this study, we examined the mode of inheritance of Indoxacarb resistance in P. xylostella. The indoxacarb-resistant strain (Px-R) was obtained through continuous laboratory selection with increasing doses of indoxacarb in each generation. At the 14th generation of selection, the resistance ratio of Px-R strains was 238 over the susceptible strain (Px-S). The mode of inheritance to Indoxacarb in P. xylostella was examined performing standard reciprocal crosses between Px-R and Px-S and response of Px-R, Px-S and F1 hybrid progenies to Indoxacarb through leaf dip bioassay. The degree of dominance (D) and heritability (h) of F1 hybrid progeny ranged from ?0.001 to 0.0012 and 0.499 to 0.506, respectively. The Indoxacarb resistance was appeared to be autosomal and inherited as a semi-dominant trait. The Px-R strain of P. xylostella showed little cross resistance to cypermethrin and there was no cross resistance to other pesticides viz., chlorpyrifos, spinosad, karanjin, xentari (Bta-Cry1C) and MVP-II (Cry1Ac). Since the Indoxacarb resistance inherited as a semi-dominant trait in P. xylostella, the sub lethal doses and frequent use of indoxacarb should be avoided for the management of P. xylostella. Moreover, Px-R of P. xylostella showed positive cross resistance to synthetic pyrethroids (cypemethrin), therefore indoxacarb and synthetic pyrethroids should not be recommended together for management of P. xylostella.     

Resistance to neonicotinoid insecticides in field populations of the Colorado potato beetle (Coleoptera: Chrysomelidae)

BACKGROUND: Neonicotinoid insecticides were first used commercially for Colorado potato beetle [Leptinotarsa decemlineata (Say), Coleoptera: Chrysomelidae] control in the United States in 1995, and since then have been critical for management of this pest. Field populations from the northeastern and midwestern United States were tested from 1998 to 2010 for susceptibility to imidacloprid and thiamethoxam using standard topical dose assays with adults. RESULTS: From 1998 to 2001, imidacloprid resistance was present in only a few locations in the eastern United States. By 2003, imidacloprid resistance was common in the northeastern Unites States. In 2004, imidacloprid resistance in Colorado potato beetle was detected for the first time in the midwestern United States. In 2003, the first case of resistance to thiamethoxam was found in a population from Massachusetts. Neonicotinoid resistance in summer‐generation adults was higher than in overwintered adults from the same locations. By 2009, 95% of the populations tested from the northeastern and midwestern United States had significantly higher LD₅₀ values for imidacloprid than the susceptible population. CONCLUSIONS: The increasing resistance to neonicotinoid insecticides raises concerns for the continued effective management of Colorado potato beetles in potatoes and highlights the need for more rigorous practice of integrated pest management methods. Copyright © 2011 Society of Chemical Industry     

小麦纹枯病抗性及抗性遗传的初步研究

 从一个多亲本的复式杂交后代中,选育了4个高抗纹枯病的小麦新品系,编号为MN-3、7、18和19。抗病性鉴定证明,在对照品种绵阳19病株率100%,发病等级4~5级的情况下,这4个新品系的病株率和发病等级分别在3.65%~6.98%和0~1之间。这4个品系与高感纹枯病的小麦品种绵阳19杂交,在F2代群体中植株符合抗:感=3:1的分离比率,在隐性亲本的测交后代中符合1:1的分离比率;在这4个品系之间的杂交后代群体中未观察到抗性的分离。试验结果指出,4个品系均含有同一个抗小麦纹枯病的单显性抗病基因,该基因被命名为Ses 1。本研究指出了小麦抗纹枯病育种的可能性,并为进一步研究小麦宿主和纹枯病菌原的相互关系及其遗传学提供了材料。     

Inheritance of resistance and cross-resistance to deltamethrin in Plutella xylostella (Lepidoptera: Plutellidae) from Pakistan

A field population of Plutella xylostella (L) from Pakistan was found to be highly resistant to deltamethrin (>500-fold) but had little or no resistance to spinosad, fipronil, indoxacarb, abamectin, Bacillus thuringiensis (Bt) var kurstaki, Bt var aizawai or Cry1Ac when compared with a susceptible laboratory population, Lab-UK. A sub-population was selected for six generations (laboratory G3-G8) with deltamethrin (delta-SEL), while a second sub-population was left unselected (UNSEL). Bioassays at G9 found that selection with deltamethrin gave resistance ratios of >230 compared with UNSEL (>6730 compared with Lab-UK). The delta-selected population showed no apparent cross-resistance to spinosad, fipronil or indoxacarb. Logit regression analysis of F1 reciprocal crosses between delta-SEL and Lab-UK indicated that resistance to deltamethrin in the delta-SEL population was inherited as an autosomal, incompletely dominant (D(LC) = 0.67) trait. A direct test of monogenic inheritance based on a back-cross of F1 progeny with delta-SEL suggested that resistance to deltamethrin was controlled by more than one factor.     

Inheritance of Resistance to Leptosphaeria maculans in Brassica juncea

ABSTRACT The inheritance of resistance to Leptosphaeria maculans, the causal agent of black leg of crucifers, was studied in Brassica juncea. Three resistant accessions (UM3021, UM3043, and UM3323) and one susceptible accession (UM3132) of B. juncea were crossed in a complete diallel. Parents, F(1), and F(2) progenies were evaluated for all crosses using both cotyledon and stem inoculation. Cotyledon reaction was evaluated with two isolates of L. maculans, but stem reaction was evaluated with one isolate. Disease reactions observed for individual plants were the same for both inoculation methods and for both isolates of the pathogen for cotyledon reaction. No segregation was observed for the crosses between resistant accessions (UM3043 x UM3323 and UM3021 x UM3323), but a few susceptible plants were observed in the F(2) progeny of crosses between resistant parents (UM3021 x UM3043). This was probably due to heterozygosity in some parental plants of UM3021. For crosses be tween the susceptible parent and resistant parents, F(1) plants for two crosses were all resistant. For cross UM3132 x UM3021, some susceptible plants occurred, which was also suggestive of heterozygosity in UM3021. Although resistance in F(1) was dominant, for F(2) populations, segregation fit either 13:3, 3:1, or 1:3 ratios, indicating that resistance can be either adominant or recessive trait. F(3) families derived from some susceptible F(2) plants from crosses UM3021 x UM3132 and UM3043 x UM3132 were evaluated using the cotyledon inoculation method only. Segregation of F(2) plants and F(3) families in crosses involving resistant and susceptible parents indicated that the resistance to L. maculans in B. juncea is controlled by two nuclear genes with dominant recessive epistatic gene action.     

Dose-response relationships for the antifeedant effects of Humulus lupulus extracts against larvae and adults of the Colorado potato beetle

BACKGROUND: Dose–response relationships for antifeedant effects of H. lupulus extracts against larvae and adults of the Colorado potato beetle (CPB) were determined in laboratory conditions. The larval and adult beetles were fed on potato leaflets treated with H. lupulus extract ranging from 0.4 to 40 mg mL^?1 in a no‐choice situation. Their feeding behavior was recorded, and larval growth and antifeedant indexes were calculated. RESULTS: H. lupulus treatments significantly affected larval growth rate, and at higher concentrations the larval weights were significantly reduced over the course of the assay. Adults of CPB were more sensitive to the extracts than the larvae, and, even at lower doses, adult beetles were arrested for longer periods than larvae. CONCLUSION: These results indicate that H. lupulus extracts may have potential for control of CPB, particularly in organic farms where conventional insecticides are not available. Copyright © 2012 Society of Chemical Industry     

Cross-resistance and inheritance of resistance to Bacillus thuringiensis toxin Cry1Ac in diamondback moth (Plutella xylostella L) from lowland Malaysia

A field population of Plutella xylostella from Malaysia (SERD4) was divided into five sub-populations and four were selected (G2-G5) with the Bacillus thuringiensis insecticidal crystal (Cry) toxins Cry1Ac, Cry1Ab, Cry1Ca and Cry1Da. Bioassay at G6 gave resistance ratios of 88, 5, 2 and 3 for Cry1Ac, Cry1Ab, Cry1Ca and Cry1Da respectively compared with the unselected sub-population (UNSEL-SERD4). The Cry1Ac-selected population showed little cross-resistance to Cry1Ab, Cry1Ca and Cry1Da, (3-, 2- and 3-fold compared with UNSEL-SERD4), whereas the Cry1Ab-SEL sub-population showed marked cross-resistance to Cry1Ac (40-fold), much greater than Cry1Ab itself. In contrast, the Cry1Ca- and Cry1Da-SEL sub-population showed little if any cross-resistance to Cry1Ac and Cry1Ab. The mode of inheritance of resistance to Cry1Ac was examined in Cry1Ac-selected SERD4 by standard reciprocal crosses and back-crosses using a laboratory insecticide-susceptible population (ROTH). Logit regression analysis of F1 reciprocal crosses indicated that resistance to Cry1Ac was inherited as an incompletely dominant trait. At the highest dose of Cry1Ac tested, resistance was recessive, while at the lowest dose it was almost completely dominant. The F2 progeny from a back-cross of F1 progeny with ROTH were tested with a concentration of Cry1Ac that would kill 100% of ROTH. The mortality ranged between 50 and 95% in seven families of back-cross progeny, which indicated that more than one allele on separate loci were responsible for resistance to Cry1Ac.     

Validation of a QTL for resistance to ascochyta blight linked to resistance to fusarium wilt race 5 in chickpea (<Emphasis Type="Italic">Cicer arietinum</Emphasis> L.)

Ascochyta blight caused by Ascochyta rabiei and fusarium wilt caused by Fusarium oxysporum. f. sp. ciceris are the two most serious diseases of chickpea (Cicer arietinum). Quantitative trait loci (QTL) or genes for ascochyta blight resistance and a cluster of resistance genes for several fusarium wilt races (foc1, foc3, foc4 and foc5) located on LG2 of the chickpea map have been reported independently. In order to validate these results and study the linkage relationship between the loci that confer resistance to blight and wilt, an intraspecific chickpea recombinant inbred lines (RIL) population that segregates for resistance to both diseases was studied. A new LG2 was established using sequence tagged microsatellite sites (STMS) markers selected from other chickpea maps. Resistance to race 5 of F. oxysporum (foc5) was inherited as a single gene and mapped to LG2, flanked by the STMS markers TA110 (6.5 cM apart) and TA59 (8.9 cM apart). A QTL for resistance to ascochyta blight (QTL_AR3) was also detected on LG2 using evaluation data obtained separately in two cropping seasons. This genomic region, where QTL_AR3 is located, was highly saturated with STMS markers. STMS TA194 appeared tightly linked to QTL_AR3 and was flanked by the STMS markers TR58 and TS82 (6.5 cM apart). The genetic distance between foc5 and QTL_AR3 peak was around 24 cM including six markers within this interval. The markers linked to both loci could facilitate the pyramiding of resistance genes for both diseases through MAS.     

Resistance and cross-resistance to neonicotinoid insecticides and spinosad in the Colorado potato beetle, Leptinotarsa decemlineata (Say) (Coleoptera: Chrysomelidae)

The Colorado potato beetle, Leptinotarsa decemlineata (Say), has developed resistance to many insecticides used for its control, recently including imidacloprid, a neonicotinoid compound. Other neonicotinoids are now being deployed to control this pest. A key point in the strategies of resistance management is the monitoring of resistance and cross-resistance. In the summer of 2003, imidacloprid-resistant adult Colorado potato beetles collected from Long Island, New York, USA were bioassayed using topical applications of imidacloprid and nine other neonicotinoids. Compared to a standard susceptible strain, the Long Island beetles showed 309-fold resistance to imidacloprid, and lower levels of cross-resistance to all other neonicotinoids, despite these never having been used in the field, i.e., 59-fold to dinotefuran, 33-fold to clothianidin, 29-fold to acetamiprid, 28-fold to N-methylimidacloprid, 25-fold to thiacloprid, 15-fold to thiamethoxam, 10-fold to nitenpyram, but less than 2-fold to nicotine. In injection bioassays, high resistance to imidacloprid was also found (116-fold). Piperonyl butoxide partially suppressed resistance to imidacloprid, but the resistance level was still over 100-fold, indicating that other mechanisms were primarily responsible for resistance. Low levels of resistance (8- to 10-fold) were found to the nicotinic activator, spinosad, in an imidacloprid-resistant strain collected from the same field in 2004. The cross-resistance seen with all the neonicotinoids tested suggests that the rotation of imidacloprid with other neonicotinoids may not be an effective long-term resistance management strategy. Rotation with spinosad also carries some risk, but it is unlikely that spinosad resistance in this case is mechanistically related to that for the neonicotinoids.     

Detection of single-base substitution in an esterase gene and its linkage to malathion resistance in the parasitoid Anisopteromalus calandrae (Hymenoptera: Pteromalidae)

Anisopteromalus calandrae (Howard) (Hymenoptera: Pteromalidae) is an important parasitoid of stored-grain insect pests. Partial cDNA sequences of an esterase-like enzyme have been obtained from a malathion-resistant (R) strain and a susceptible (S) strain of this wasp. A single-base substitution in the R strain has been confirmed by using PCR amplification of specific allele (PASA) to amplify genomic DNA extracted from individual resistant and susceptible parents, F₁ hybrids from double reciprocal crosses, and progeny from backcrosses. The R allele appeared to be inherited in a strict Mendelian fashion in both diploid female and haploid male progeny. The esterase fragment co-segregated with resistance in these crosses and backcrosses. Female wasps in a mixed population of A calandrae that survived a malathion screen carried the R allele for the esterase-like enzyme, while those wasps that died did not have the R allele. The single base-pair mutation, guanine in the R strain and thymine in the S strain, presumably results in a tryptophan-to-glycine amino acid substitution in the encoded protein. We do not know how these amino acid substitutions may relate to functional differences in the enzyme. However, this esterase gene or another linked esterase gene may encode the resistance-associated malathion detoxifying activity in the R strain. © 1999 Society of Chemical Industry     

Genetics of spinosad resistance in a multi-resistant field-selected population of Plutella xylostella

Resistance to the bacteria-derived insecticides spinosad (Conserve), abamectin (Vertimec), Bacillus thuringiensis var kurstaki (Btk) (Dipel), B thuringiensis var aizawai (Bta) (Xentari), B thuringiensis crystal endotoxins Cry1Ac and Cry1Ca, and to the synthetic insecticide fipronil was estimated in a freshly-collected field population (CH1 strain) of Plutella xylostella (L) from the Cameron Highlands, Malaysia. Laboratory bioassays at G1 indicated significant levels of resistance to spinosad, abamectin, Cry1Ac, Btk, Cry1Ca, fipronil and Bta when compared with a laboratory insecticide-susceptible population. Logit regression analysis of F1 reciprocal crosses indicated that resistance to spinosad in the CH1 population was inherited as a co-dominant trait. At the highest dose of spinosad tested, resistance was close to completely recessive, while at the lowest dose it was incompletely dominant. A direct test of monogenic inheritance based on a back-cross of F1 progeny with CH1 suggested that resistance to spinosad was controlled by a single locus.     

Variability and selection of verticillium wilt resistant genotypes in cultivated olive and in the Olea genus

Developing verticillium wilt resistant genotypes is currently a major objective in olive breeding. In this study, 6017 genotypes derived from 48 crosses obtained by open pollination and crosses between olive cultivars, wild olive genotypes and other Olea species and Olea europaea subspecies were individually evaluated for verticillium wilt resistance. More than 800 genotypes were identified as resistant to the disease based on the absence of symptoms. High genetic variability and wide segregation in resistance were observed. The inheritance of resistance was studied, and the best parents and crosses to breed resistant genotypes were identified. According to the results, verticillium wilt resistance in olive appears to be a quantitative trait. The results obtained by comparing the level of resistance between different crosses as well as by estimating heritability suggest that it is possible to breed for verticillium wilt resistance in olive.     

Mutations in the mitochondrial cytochrome b of Tetranychus urticae Koch (Acari: Tetranychidae) confer cross‐resistance between bifenazate and acequinocyl

BACKGROUND: Resistance of Tetranychus urticae Koch to bifenazate was recently linked with mutations in the mitochondrial cytochrome b Q_o pocket, suggesting that bifenazate acts as a Q_o inhibitor (Q_oI). Since these mutations might cause cross‐resistance to the known acaricidal Q_oI acequinocyl and fluacrypyrim, resistance levels and inheritance patterns were investigated in several bifenazate‐susceptible and bifenazate‐resistant strains with different mutations in the cd1 and ef helices aligning the Q_o pocket. RESULTS: Cross‐resistance to acequinocyl in two bifenazate‐resistant strains was shown to be maternally inherited and caused by the combination of two specific mutations in the cytochrome b Q_o pocket. Although most investigated strains were resistant to fluacrypyrim, resistance was not inherited maternally, but as a monogenic autosomal highly dominant trait. As a consequence, there was no correlation between cytochrome b genotype and fluacrypyrim resistance. CONCLUSIONS: Although there is no absolute cross‐resistance between bifenazate, acequinocyl and fluacrypyrim, some bifenazate resistance mutations confer cross‐resistance to acequinocyl. In the light of resistance development and management, high prudence is called for when alternating bifenazate and acequinocyl in the same crop. Maternally inherited cross‐resistance between bifenazate and acequinocyl reinforces the likelihood of bifenazate acting as a mitochondrial complex III inhibitor at the Q_o site. Copyright © 2009 Society of Chemical Industry