New mutation increases resistance of Myzus persicae to neonicotinoids

Study links R81S and V101I to high levels of resistance and points to the involvement of detoxification enzymes

10.09.2026 | 09:54 (UTC -3)
Cultivar Magazine
doi 10.1016/j.pestbp.2026.107338
doi 10.1016/j.pestbp.2026.107338

Researchers have identified a new mutation linked to neonicotinoid resistance in peach orchards in Beijing, China, using the nicotinic acetylcholine receptor nAChR beta1, called Myzus persicae. The R81S substitution occurred alongside the V101I mutation. This combination increased resistance to insecticides of different generations.

The study evaluated six populations collected in 2025 (doi 10.1016/j.pestbp.2026.107338). Bioassays recorded resistance of 15,99 to 30,97 times to imidacloprid, 9,16 to 50,79 times to acetamiprid, 1,28 to 25,26 times to sulfoxaflor, 6,12 to 16,95 times to thiamethoxam, and 6,63 to 12,27 times to dinotefuran.

Genetic analysis

Genetic analysis found the already known R81T and V101I mutations, in addition to the new R81S mutation. The isolated V101I mutation appeared in 69,75% of individuals. Combinations of R81T or R81S with V101I occurred in 22,56%.

Monoclonal strains allowed the effect of the genotypes to be separated. The isolated V101I strain provided resistance between 13,73 and 394,21 times. The R81T/S+V101I combinations reached between 73,10 and more than 1.146,79 times.

Another relationship

The study also linked resistance to increased activity of cytochrome P450, glutathione S-transferase, and carboxylesterase. Assays with synergists indicated greater involvement of P450 enzymes. Molecular simulations showed alterations in the nAChR binding site and reduced affinity for imidacloprid in the combined mutations.

Researchers point to a combined action of mutations in the target and metabolic mechanisms. The results reinforce the need for resistance monitoring and rotation of insecticides with different modes of action.

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