Biochemical Markers Linked to Abamectin Resistance in Tetranychus urticae (Acari: Tetranychidae)

Stumpf, Natascha; Nauen, Ralf

doi:10.1006/pest.2001.2583

Cited by 229 publications

(192 citation statements)

References 20 publications

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“…Although the abamectin resistance frequency decreased from 75% to less than 15% in six months in our population of T. urticae, abamectin resistance was shown to be stable in the laboratory at least over six months in a Dutch strain (NL-00) of two-spotted spider mite, collected from roses (Stumpf & Nauen 2002). These reports indicate that the instability of abamectin resistance can not be generalized for all populations of T. urticae in Brazil.…”

Section: Discussioncontrasting

confidence: 56%

“…Stumpf & Nauen (2002), investigating enzymes involved in abamectin resistance in the two-spotted spider mite, observed that resistant strains (NL-00 and COL-00) presented severalfold higher MFO (cytochrome P450-dependent monooxygenase) activity than the susceptible strain GSS. Abamectin resistance in strain NL-00 was strongly synergized by PBO (piperonyl butoxide) and DEM (diethyl maleate), suggesting that MFO and GST (glutathione S-transferases) may be involved in abamectin resistance (Stumpf & Nauen 2002).…”

Section: Discussionmentioning

confidence: 99%

“…Stability of acaricide resistance has been studied for several compounds in T. urticae and other species of mites (Inoue 1980, Sato et al 2004, Stumpf & Nauen 2002. Dicofol resistance was shown to be unstable in Panonychus citri (McGregor), in the absence of selection pressure (Inoue 1980).…”

Section: Discussionmentioning

confidence: 99%

“…Recently, some growers have observed low efficacy and shortened residual control with abamectin, indicating a possible problem of resistance development. Although various aspects of abamectin resistance in T. urticae have been studied during the last ten years (Campos et al 1995, 1996, Beers et al 1998, Stumpf & Nauen 2002, there is no information about abamectin resistance in this pest in Brazil.…”

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Abamectin resistance in Tetranychus urticae Koch (Acari: Tetranychidae): selection, cross-resistance and stability of resistance

Sato¹,

Silva²,

Raga³

et al. 2005

Neotrop. Entomol.

133

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Neotropical Entomology 34(6): 991-998 (2005) Resistência de PALAVRAS-CHAVE: Ácaro rajado, manejo da resistência, controle químico ABSTRACT -Studies on artificial laboratory selections with abamectin, cross-resistance relationships, and stability of resistance were carried out with Tetranychus urticae Koch to provide basic information for an abamectin resistance management program. Selections for resistance and susceptibility to abamectin were performed in a population of T. urticae, collected from a commercial strawberry field in the State of São Paulo, Brazil. After five selections for resistance and five selections for susceptibility, susceptible (S) and resistant (R) strains of T. urticae to abamectin were obtained. The resistance ratio (R/S) at the LC 50 reached 342-fold values. The toxicity of eight acaricides was evaluated in the R and S strains, observing significant differences (at LC 50 ) between R and S strains for milbemectin, fenpropathrin and chlorfenapyr. Significant correlation was detected between the LC 50 s of abamectin and milbemectin, indicating cross-resistance between these acaricides. No crossresistance was detected for the acaricides fenpyroximate, cyhexatin, propargite and dimethoate. The stability of abamectin resistance was also studied under laboratory conditions. Abamectin resistance was unstable in the absence of selection pressure. For all studied populations (with 75, 50 and 25% of initial frequency of resistant mites), the percentage of resistant mites decreased to levels equal or lower than 15% in six months. The results indicate that milbemectin should be avoided for managing abamectin resistance in T. urticae.

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Section: Discussioncontrasting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Abamectin resistance in Tetranychus urticae Koch (Acari: Tetranychidae): selection, cross-resistance and stability of resistance

Sato¹,

Silva²,

Raga³

et al. 2005

Neotrop. Entomol.

133

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“…Reports of abamectin/milbemectin field resistance remain relatively scarce for T. urticae , despite the heavy use of both compounds against spider mite infestations for more than 30 years (Campos, Dybas, & Krupa, 1995; Campos, Krupa, & Dybas, 1996; Kwon, Lee, Ahn, & Lee, 2014; Stumpf & Nauen, 2002; Van Leeuwen et al., 2010). Abamectin resistance is known to evolve through different mechanisms and can include target‐site and/or biochemical/metabolic resistance (Dermauw et al., 2012; Kwon, Yoon, et al., 2010; Pavlidi et al., 2015; Riga et al., 2014, 2017).…”

Section: Discussionmentioning

confidence: 99%

Fitness costs of key point mutations that underlie acaricide target‐site resistance in the two‐spotted spider miteTetranychus urticae

Bajda

Riga

Wybouw

et al. 2018

Evolutionary Applications

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The frequency of insecticide/acaricide target‐site resistance is increasing in arthropod pest populations and is typically underpinned by single point mutations that affect the binding strength between the insecticide/acaricide and its target‐site. Theory predicts that although resistance mutations clearly have advantageous effects under the selection pressure of the insecticide/acaricide, they might convey negative pleiotropic effects on other aspects of fitness. If such fitness costs are in place, target‐site resistance is thus likely to disappear in the absence of insecticide/acaricide treatment, a process that would counteract the spread of resistance in agricultural crops. Hence, there is a great need to reliably quantify the various potential pleiotropic effects of target‐site resistance point mutations on arthropod fitness. Here, we used near‐isogenic lines of the spider mite pest Tetranychus urticae that carry well‐characterized acaricide target‐site resistance mutations to quantify potential fitness costs. Specifically, we analyzed P262T in the mitochondrial cytochrome b, the combined G314D and G326E substitutions in the glutamate‐gated chloride channels, L1024V in the voltage‐gated sodium channel, and I1017F in chitin synthase 1. Five fertility life table parameters and nine single‐generation life‐history traits were quantified and compared across a total of 15 mite lines. In addition, we monitored the temporal resistance level dynamics of populations with different starting frequency levels of the chitin synthase resistant allele to further support our findings. Three target‐site resistance mutations, I1017F and the co‐occurring G314D and G326E mutations, were shown to significantly and consistently alter certain fitness parameters in T. urticae. The other two mutations (P262T and L1024V) did not result in any consistent change in a fitness parameter analyzed in our study. Our findings are discussed in the context of the global spread of T. urticae pesticide resistance and integrated pest management.

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Identification of biochemical markers linked to neonicotinoid cross resistance in Bemisia tabaci (Hemiptera: Aleyrodidae)

Rauch

Nauen

2003

Arch Insect Biochem Physiol

Self Cite

245

243

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The whitefly, Bemisia tabaci (Hemiptera: Aleyrodidae), is a serious pest in many cropping systems world-wide and occurs in different biotypes. The most widespread one is the B-type, whereas the Q-biotype is nowadays still mostly restricted to Southern Spain. Neonicotinoid cross-resistance is known at a high level in Q-types from Spain and individual samples collected in Italy and Germany. Now we detected for the first time high neonicotinoid cross-resistance in a B-type from Israel. Target site resistance to imidacloprid using [(3)H]imidacloprid in nicotinic acetylcholine receptor (nAChR) binding assays could not be detected in any of these highly resistant strains. The impact of metabolizing enzymes such as esterases, glutathione S-transferases, and cytochrome P450-dependent monooxygenases in neonicotinoid resistance was studied biochemically with artificial substrates. Monooxygenase activity was increased 2-3-fold in moderately resistant strains (RF approximately 30) and even 5-6-fold in highly resistant strains (RF approximately 1,000). Only monooxygenase activity correlated with imidacloprid, thiamethoxam and acetamiprid resistance and, therefore, monooxygenases seem to be the only enzyme system responsible for neonicotinoid resistance in B. tabaci Q- and B-types. The oxidative degradation of imidacloprid in resistant Q-type strains could be confirmed by metabolism studies of [(14)C]imidacloprid in vivo. Five-hydroxy-imidacloprid could be detected as the only main metabolite. The insecticidal activity and binding affinity to nAChR of this compound was 10 times lower than imidacloprid itself in B. tabaci.

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Biochemical Markers Linked to Abamectin Resistance in Tetranychus urticae (Acari: Tetranychidae)

Cited by 229 publications

References 20 publications

Abamectin resistance in Tetranychus urticae Koch (Acari: Tetranychidae): selection, cross-resistance and stability of resistance

Abamectin resistance in Tetranychus urticae Koch (Acari: Tetranychidae): selection, cross-resistance and stability of resistance

Fitness costs of key point mutations that underlie acaricide target‐site resistance in the two‐spotted spider miteTetranychus urticae

Identification of biochemical markers linked to neonicotinoid cross resistance in Bemisia tabaci (Hemiptera: Aleyrodidae)

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