Geographical distribution and molecular insights into abamectin and milbemectin cross-resistance in European field populations of Tetranychus urticae.

BACKGROUND

Milbemectin and abamectin are frequently used to control the spider mite Tetranychus urticae. The development of abamectin resistance in this major pest has become an increasing problem worldwide, potentially compromising the use of milbemectin. In this study, a large collection of European field populations was screened for milbemectin and abamectin resistance, and both target-site and metabolic (cross-)resistance mechanisms were investigated.

RESULTS

High to very high levels of abamectin resistance were found in one third of all populations, while milbemectin resistance levels were low for most populations. The occurrence of well-known target-site resistance mutations in glutamate-gated chloride channels (G314D in GluCl1 and G326E in GluCl3) was documented in the most resistant populations. However, a new mutation, I321T in GluCl3, was also uncovered in three resistant populations, while a V327G and L329F mutation was found in GluCl3 of one resistant population. A differential gene-expression analysis revealed the overexpression of detoxification genes, more specifically cytochrome P450 monooxygenase (P450) and UDP-glycosyltransferase (UGT) genes. Multiple UGTs were functionally expressed, and their capability to glycosylate abamectin and milbemectin, was tested and confirmed.

CONCLUSIONS

We found a clear correlation between abamectin and milbemectin resistance in European T. urticae populations, but as milbemectin resistance levels were low, the observed cross-resistance is probably not of operational importance. The presence of target-site resistance mutations in GluCl genes was confirmed in most but not all resistant populations. Gene-expression analysis and functional characterization of P450s and UGTs suggests that also metabolic abamectin resistance mechanisms are common in European T. urticae populations. © 2020 Society of Chemical Industry.