Intraspecific diversity in the mechanisms underlying abamectin resistance in a cosmopolitan pest

Abstract

Pesticide resistance relies on a myriad of mechanisms, ranging from single mutations to a complex and polygenic architecture, and it involves mechanisms such as target-site insensitivity, metabolic detoxification, or a combination of these, with either additive or synergistic effects. Several resistance mechanisms against abamectin, a macrocyclic lactone widely used in crop protection, have been reported in the cosmopolitan pest Tetranychus urticae. However, it has been shown that a single mechanism cannot account for the high levels of abamectin resistance found across different mite populations. Here, we used experimental evolution combined with bulked segregant analyses to map quantitative trait loci (QTL) associated with abamectin resistance in two genetically unrelated strains of T. urticae. In these two independent QTL mapping experiments, three and four QTLs were identified, of which three were shared between experiments. Shared QTLs contained genes encoding subunits of the glutamate-gated chloride channel (GluCl) and harboured previously reported mutations, including G314D in GluCl1 and G326E in GluCl3, but also novel resistance candidate loci, including DNA helicases and chemosensory receptors. Surprisingly, the fourth QTL, present only in only one of the experiments and thus unique for one parental resistant strain, revealed a non-functional variant of GluCl2, suggesting gene knock-out as resistance mechanism. Our study uncovers the complex basis of abamectin resistance, and it highlights the intraspecific diversity of genetic mechanisms underlying resistance in a cosmopolitan pest.

Cross‐resistance, inheritance and biochemical mechanism of abamectin resistance in a field‐derived strain of the citrus red mite, Panonychus citri (Acari: Tetranychidae)

“…26,47,49 Moreover, high-resolution QTL mapping revealed a polygenic basis associated with abamectin resistance in T. urticae. 50 The development of pesticide resistance mediated by multiple genes was slower than that of monogenic resistance. 51,52 Moreover, resistance controlled by multiple genes often leads to cross-resistance in arthropod pests.…”

Independent genetic mapping experiments identify diverse molecular determinants of host adaptation in a generalist herbivore

“…In addition, a wellannotated, chromosome-level assembled genome facilitates the integration of bioassays with genomic tools to identify causal genes within quantitative trait loci (QTLs) (Grbić et al, 2011;Kurlovs et al, 2019;Wybouw et al, 2019). For example, bulked segregant analyses (BSA) paired with whole genome sequencing have successfully mapped QTL regions underlying resistance to multiple classes of acaricides Vandenhole et al, 2023;Villacis-Perez et al, 2023;Wybouw et al, 2019). However, the identification of loci that respond to selection imposed by host plants remains elusive.…”

The complex II resistance mutation H258Y in succinate dehydrogenase subunit B causes fitness penalties associated with mitochondrial respiratory deficiency

“…The spider mite Tetranychus urticae is a major agricultural pest that quickly develops resistance to pesticides of varying modes of action. The resistance traits are often complex, involving a combination of multiple factors 21–26 . In most resistance cases, both metabolic detoxification genes and target‐site mutations have been identified in the resistant phenotypes 2,4,22,27 .…”

“…The resistance traits are often complex, involving a combination of multiple factors. [21][22][23][24][25][26] In most resistance cases, both metabolic detoxification genes and target-site mutations have been identified in the resistant phenotypes. 2,4,22,27 By carrying out repeated backcrossing, a number of target site mutations have been uncoupled from other mechanisms and their relative contribution to resistance assessed.…”