Acaricide resistance and resistance mechanisms in Tetranychus urticae populations from rose greenhouses in the Netherlands.

BACKGROUND: Spider mites are important crop pests that rapidly develop resistance to acaricides. To investigate whether acaricide resistance is a threat to greenhouse rose culture in the Netherlands, the susceptibility of 15 strains of Tetranychus urticae was tested to several currently used acaricides, and resistance mechanisms were investigated. RESULTS: Although the observed levels of susceptibility differed between strains and acaricides, resistance was detected in most strains. The activity of detoxifying enzymes was significantly increased in most field-collected strains, and a number of amino acid substitutions known to be involved in resistance were detected. CONCLUSIONS: Resistance levels to traditional acaricides such as bifenthrin and abamectin were prominent, and might result in control failure under field conditions. Resistance to more recently registered compounds was detected in several populations. Resistance levels were generally unstable in the laboratory without selection pressure. The toxicological, biochemical and genetic data in this study will be essential in devising an efficient resistant management for Dutch rose culture.

Development of acaricide resistance in Pacific spider mite (Tetranychus pacificus) from California vineyards.

In recent years, grape growers in California reported failures of acaricides against Tetranychus pacificus McGregor. We collected T. pacificus populations from four vineyards and tested them for resistance to bifenazate, propargite and pyridaben. In addition, we sequenced part of the cytochrome b gene of bifenazate-resistant and -susceptible T. pacificus to test for the presence of mutations reported to confer resistance to the congeneric T. urticae. None of the mutations conferring resistance to bifenazate in T. urticae were present in resistant T. pacificus. Resistance levels ranged from full susceptibility to statistically significant 11-fold resistance to pyridaben, sevenfold resistance to bifenazate and fourfold resistance to propargite compared to a susceptible population. Despite the relatively low levels of resistance detected, we estimated that under the conditions of our study the highest field rates of bifenazate and pyridaben application would cause less than 58 and 66% mortality of adult females in the most resistant populations, respectively. In contrast, field rates of propargite application would cause close to 100% mortality in the least susceptible population. These results highlight a potential link between resistance development and reduced field effectiveness for bifenazate and pyridaben. Finally, T. pacificus may be more tolerant to bifenazate and propargite than T. urticae, since the LC(50) values for the susceptible population of T. pacificus were several times higher than LC(50)'s reported for susceptible T. urticae.

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(o)I). Since these mutations might cause cross-resistance to the known acaricidal Q(o)I 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.

Mitochondrial heteroplasmy and the evolution of insecticide resistance: non-Mendelian inheritance in action.

Genes encoded by mitochondrial DNA (mtDNA) exist in large numbers per cell but can be selected very rapidly as a result of unequal partitioning of mtDNA between germ cells during embryogenesis. However, empirical studies of this "bottlenecking" effect are rare because of the apparent scarcity of heteroplasmic individuals possessing more than one mtDNA haplotype. Here, we report an example of insecticide resistance in an arthropod pest (Tetranychus urticae) being controlled by mtDNA and on its inheritance in a heteroplasmic mite strain. Resistance to the insecticide bifenazate is highly correlated with remarkable mutations in cytochrome b, a mitochondrially encoded protein in the respiratory pathway. Four sites in the Q(o) site that are absolutely conserved across fungi, protozoa, plants, and animals are mutated in resistant mite strains. Despite the unusual nature of these mutations, resistant mites showed no fitness costs in the absence of insecticide. Partially resistant strains, consisting of heteroplasmic individuals, transmit their resistant and susceptible haplotypes to progeny in highly variable ratios consistent with a sampling bottleneck of approximately 180 copies. Insecticide selection on heteroplasmic individuals favors those carrying resistant haplotypes at a frequency of 60% or more. This combination of factors enables very rapid evolution and accounts for mutations being fixed in most field-collected resistant strains. The results provide a rare insight into non-Mendelian mechanisms of mitochondrial inheritance and evolution, relevant to anticipating and understanding the development of other mitochondrially encoded adaptations in arthropods. They also provide strong evidence of cytochrome b being the target site for bifenazate in spider mites.