Unprecedented mutation threatens effectiveness of acaricides in greenhouses

Mite populations Tetranychus urticae have developed resistance to acaricides used in the management of horticultural and ornamental crops in Turkey. The resistance involves a new mutation in the mitochondrial gene and the increase in enzymes that degrade pesticides. The finding raises a warning for producers who depend on acaricides from the group of respiratory chain complex III inhibitors.

Acequinocil and bifenazate are the main compounds in this class. Both act on mitochondria, interrupting energy production. They are preferred in protected cultivation systems because they have low toxicity to natural enemies.

However, tests with populations of T. urticae revealed resistance in four of the twelve samples evaluated. The resistance levels exceeded the expected limits for effective control in the field, explain the researchers who worked on the study.

New mitochondrial mutation detected

Populations from ornamental greenhouses showed extreme levels of resistance. Molecular analyses revealed the presence of a novel mutation, M128T, in a conserved region of cytochrome b, a key protein of mitochondrial complex III. The mutation was fixed in populations subjected to selection with acequinocyl.

Reciprocal cross tests between resistant and susceptible lines confirmed the maternal inheritance of resistance. The result indicates direct involvement of mitochondrial mutation.

Nevertheless, the resistance conferred by M128T was moderate. This suggests that other mechanisms also contribute to the reduction in the efficacy of acaricides.

Enzymatic activity increases resistance

Transcriptomic analyses of resistant populations revealed overexpression of genes related to detoxification.

Among them, P450-type monooxygenases, esterases (CCE) and DOG enzymes (dioxygenases) stand out, associated with the degradation of toxic compounds. The Tu4S population, the most resistant among those tested, showed an increase in the activity of P450 enzymes and CCEs.

Tests with chemical synergists confirmed the role of P450s in resistance. When inhibited, there was an increase in the toxicity of acaricides, especially in populations with intermediate resistance. However, the efficacy of synergists was limited in highly resistant populations, indicating a set of factors acting in synergy.

Cross-effect and multiple resistance

Selection with acequinocyl also increased resistance to bifenazate, suggesting cross-resistance between the compounds.

The tests showed a direct correlation between the levels of resistance to both products. However, for other acaricides, such as abamectin and pyridaben, resistance remained stable, indicating that the mechanisms were already present in the initial populations.

Resistant populations also presented mutations associated with resistance to other modes of action, such as H92R in mitochondrial complex I. This genetic combination makes chemical management more difficult and reinforces the need for integrated strategies.

Recommendations for management

The research recommends constant monitoring of populations of T. urticae regarding the presence of the M128T mutation. The mutation can serve as a molecular marker for early diagnosis of resistance.

Furthermore, the researchers suggest the rotation of molecules with distinct modes of action and the use of biological agents, integrating tools in the context of integrated pest management (IPM).

Further information at doi.org/10.1016/j.pestbp.2025.106541