Academic journal article Genetics

Long-Term Population Studies Uncover the Genome Structure and Genetic Basis of Xenobiotic and Host Plant Adaptation in the Herbivore Tetranychus Urticae

Academic journal article Genetics

Long-Term Population Studies Uncover the Genome Structure and Genetic Basis of Xenobiotic and Host Plant Adaptation in the Herbivore Tetranychus Urticae

Article excerpt

Pesticides with diverse modes of action have been developed to combat populations of insect and mite herbivores, but the evolution of resistance is common. As early as 1937, Theodosius Dobzhansky noted that the emergence of resistance to chemical pesticides in insect populations was "probably the best proof of the effectiveness of natural selection yet obtained" (Dobzhansky 1937; Ceccatti 2009). In the intervening years, numerous studies have implicated genetic variants in the molecular targets of pesticides as underlying "target-site" resistance. A second major route to resistance involves genetic changes that affect penetration, metabolism, sequestration, and excretion of pesticides (toxicokinetic resistance) (Feyereisen et al. 2015). Of these, metabolic mechanisms have been especially well studied, and genetic changes affecting the coding sequences and transcription of genes in detoxification families, like cytochrome P450 monooxygenases (CYPs) and carboxyl/cholinesterases (CCEs), have been implicated in the metabolism of xenobiotics in diverse organisms (Li etai. 2007; Feyereisen etai. 2015; Van Leeuwen and Dermauw 2016).

Despite the ubiquity of pesticide resistance across arthropod species (Sparks and Nauen 2015), as well as progress in understanding the molecular mechanisms of toxicokinetic processes, questions about the genetic architecture and evolutionary origins of pesticide resistance remain (Hawkins et ai. 2018). Numerous studies have shown that the genetic architecture of resistance in herbivores can be variable (ffrench-Constant et ai. 2004; Van Leeuwen et ai. 2010; Feyereisen et ai. 2015). In some cases, a monogenic change, typically in a target-site, leads to high resistance levels observed in field populations (Roush and McKenzie 1987; Van Leeuwen et ai. 2008, 2012; Douris et ai. 2016; Riga et ai. 2017). Nevertheless, high-level resistance to pesticides in herbivore populations is often polygenic, and in most cases the number of causal loci, their relative effect sizes, the nature of the underlying loci and alleles, and their origins, are unknown (Li et ai. 2007; Hawkins et ai. 2018). More generally, detailed understandings of the genetic architecture of resistance in arthropods come disproportionally from insects like Drosophila meianogaster or mosquito species, for which discovery of resistance loci has been facilitated by dense genetic and genomic resources (ffrench-Constant et ai. 2004; Hemingway et ai. 2004; Ranson et ai. 2004). In contrast, for most herbivores, even major global pests, these resources are minimal or absent. In addition, the life histories or breeding systems of many herbivores hamper genetic approaches. Although large-effect quantitative trait loci (QTL) for resistance have been mapped in some arthropod herbivores, they frequently encompass large chromosomal regions (Gahan 2001; Saavedra-Rodriguez et ai. 2008; Coates and Siegfried 2015; Coates et ai. 2016).

Therefore, inferences about mechanisms of pesticide resistance in herbivore populations have often come from other approaches. For instance, expression studies have frequently been employed to identify genes induced or constitutively overexpressed in pesticide resistant strains (Oppenheim et ai 2015). Where resulting candidate genes are amenable to functional assays, as for CYPs and CCEs, enzymatic modification of pesticides in vitro has often been taken to suggest causality. Nonetheless, whether such candidates contribute to resistance in vivo, and their relative contribution in the case of polygenic resistance, is generally not known. Further, expression studies typically identify hundreds of candidate genes, many of which have unknown functions (Grbic et ai. 2011; Dermauw et ai 2013; Bansal et ai. 2014), or alternatively belong to gene families for which heterologous assays are either challenging or not established. The skewed focus on genes in a small number of experimentally tractable detoxification families has therefore potentially led to a biased view of the spectra of loci that contribute to pesticide resistance. …

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