Correlated responses to neonicotinoid insecticides in clones of the peach‐potato aphid, <i>Myzus persicae</i> (Hemiptera: Aphididae)

Foster, S. P.; Cox, D.; Oliphant, L.; Mitchinson, S.; Denholm, I.

doi:10.1002/ps.1648

Cited by 51 publications

(51 citation statements)

References 19 publications

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“…However, there was some cross resistance with other first-generation neonicotinoids (27). Some issues have arisen in the control of other pests; however, most reported cases of resistance have been relatively manageable or geographically localized, and most targeted insects have not shown resistance problems despite the widespread use of neonicotinoids (1,11,13,17,24,25,28,36). Although resistance problems with neonicotinoids have been manageable, we need to remain vigilant about resistance to neonicotinoids.…”

Section: Discussionmentioning

confidence: 99%

Management of Severe Curly Top in Sugar Beet with Insecticides

Strausbaugh

Wenninger

Eujayl³

2012

Plant Disease

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Curly top, caused by Curtovirus spp., is a widespread disease problem vectored by the beet leafhopper in semiarid sugar beet production areas. The insecticide seed treatment Poncho Beta has proven to be effective in controlling curly top in sugar beet but was only evaluated under light to moderate disease pressure. Thus, the insecticide seed treatments Poncho Beta, NipsIt INSIDE, and Cruiser Force were evaluated under severe curly top pressure (six viruliferous beet leafhoppers per plant) in field studies during the 2010 and 2011 growing seasons on two commercial sugar beet cultivars. In addition, the foliar insecticides Movento, Provado, and Scorpion were also evaluated. The seed treatments and Scorpion reduced curly top symptoms by 33 to 41% (P < 0.0001) and increased root yield by 55 to 95% (P < 0.0001), sucrose content by 6.5 to 7.2% (P = 0.0013 to <0.0001), and estimated recoverable sucrose by 58 to 96% (P < 0.0001) when compared with the untreated check. Movento and Provado did not improve control beyond that provided by Poncho Beta. Even under severe disease pressure 50 to 55 days after planting, neonicotinoid seed treatments can effectively reduce curly top, increase yield, and help protect against early-season insect pest pressure.Curly top in sugar beet semiarid production areas of the United States is caused by one of three Curtovirus spp. (29,35): Beet severe curly top virus (BSCTV), Beet mild curly top virus (BMCTV), and Beet curly top virus (BCTV). However, the number of Curtovirus spp. or proposed species has increased in recent years and some have been shown to occur on sugar beet in other countries (5,7,14,15,19,39). Finding more than one of the Curtovirus spp. (BCTV, BMCTV, and BSCTV) in a sugar beet plant is not uncommon (35). The virus species that cause curly top are vectored by the beet leafhopper, Circulifer tenellus Baker (Hemiptera: Cicadellidae) (3). Adult female beet leafhoppers overwinter on sagebrush steppe vegetation and weeds in desert areas and poorly managed residential areas near sugar beet fields (3,4). Overwintered females lay eggs in the spring, leading to the start of approximately three generations under Idaho conditions (3). In warmer semiarid production areas of the United States, additional beet leafhopper generations may occur. When winter host plants desiccate in the spring, the beet leafhoppers move into crop areas carrying the curly top viruses (3,4,8). Although the beet leafhopper is polyphagous and has many hosts, sugar beet is a preferred host (3,16). If the beet leafhopper migrates early in the season and a sugar beet plant is infected at an early growth stage, curly top damage is worse than if infection occurs at later growth stages (10,26,38).Sugar beet cultivars with resistance to curly top became commercially available in the mid-1930s, prior to which curly top almost eliminated the sugar beet industry in the western United States (3,4). However, resistance in sugar beet cultivars tends to be low to intermediate (31). Resistance to curly top in sugar beet is ...

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Section: Discussionmentioning

confidence: 99%

Management of Severe Curly Top in Sugar Beet with Insecticides

Strausbaugh

Wenninger

Eujayl³

2012

Plant Disease

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“…Furthermore, CYP6CY3 expression levels were significantly correlated with observed mortality after feeding on 200 ppm nicotine (R 2 = 0.91, P = 0.0003). Interestingly, CYP6CY3 was overexpressed in two M. persicae nicotianae clones, JR and 926B, that have been shown previously to be resistant to neonicotinoid insecticides (21,22). Significantly, both of these clones were collected and established before the introduction of neonicotinoids in 1991 (21,22), indicating that CYP6CY3 overexpression has not evolved as a result of selection from this insecticide class but rather may have evolved to allow enhanced detoxification of nicotine during adaptation to tobacco.…”

Section: Significancementioning

confidence: 96%

“…Five tobacco-adapted clones of M. persicae nicotianae (5410R, T25, JR, 926B, and 5191A) and three unadapted clones of M. persicae s.s. (4106A, NS, and 4255A) of diverse geographic origin were used in this study (Materials and Methods). Several of the M. persicae nicotianae clones have been shown to be resistant to nicotine and/or neonicotinoids previously (11,(21)(22)(23)). We used an artificial feeding bioassay to confirm that all M. persicae nicotianae clones are able to survive for 144 h on a diet containing 30 ppm nicotine.…”

Section: Significancementioning

confidence: 99%

Gene amplification and microsatellite polymorphism underlie a recent insect host shift

Bass

Zimmer

Riveron

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

202

192

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Host plant shifts of herbivorous insects may be a first step toward sympatric speciation and can create new pests of agriculturally important crops; however, the molecular mechanisms that mediate this process are poorly understood. Certain races of the polyphagous aphid Myzus persicae have recently adapted to feed on tobacco (Myzus persicae nicotianae) and show a reduced sensitivity to the plant alkaloid nicotine and cross-resistance to neonicotinoids a class of synthetic insecticides widely used for control. Here we show constitutive overexpression of a cytochrome P450 (CYP6CY3) allows tobacco-adapted races of M. persicae to efficiently detoxify nicotine and has preadapted them to resist neonicotinoid insecticides. CYP6CY3, is highly overexpressed in M. persicae nicotianae clones from three continents compared with M. persicae s.s. and expression level is significantly correlated with tolerance to nicotine. CYP6CY3 is highly efficient (compared with the primary human nicotine-metabolizing P450) at metabolizing nicotine and neonicotinoids to less toxic metabolites in vitro and generation of transgenic Drosophila expressing CYP6CY3 demonstrate that it confers resistance to both compounds in vivo. Overexpression of CYP6CY3 results from the expansion of a dinucleotide microsatellite in the promoter region and a recent gene amplification, with some aphid clones carrying up to 100 copies. We conclude that the mutations leading to overexpression of CYP6CY3 were a prerequisite for the host shift of M. persicae to tobacco and that gene amplification and microsatellite polymorphism are evolutionary drivers in insect host adaptation.T oxic secondary metabolites produced by many plant species present barriers to host range expansion by phytophagous insects, and the evolution of mechanisms to circumvent or detoxify these antiherbivore defenses is often a prerequisite for a successful host shift (1-3). Several studies have elucidated the molecular basis of insect adaptation to plant allelochemicals (4-7); however, most of these studies have examined adaptation that has occurred over a long evolutionary time scale and so have been unable to make direct comparisons with nonadapted conspecific races. As a result, identifying the initial genetic changes that enable a host shift has proved elusive. The recent host shift to tobacco (Nicotiana tabacum) by the peach-potato aphid, Myzus persicae, represents one of the few opportunities to study this evolutionary process in action (8). M. persicae is a globally distributed highly polyphagous aphid with a host range of >400 species, including many economically important crop plants (9). Tobacco-adapted races, Myzus persicae nicotianae, are morphologically and genetically differentiated from M. persicae sensu stricto (s.s.), although there are clear examples of recent gene flow between the two taxa (10). M. persicae nicotianae have evolved enhanced tolerance to the pyridine alkaloid nicotine (11), a potent natural insecticide produced by tobacco and other members of the Solanaceae famil...

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“…Neonicotinoid resistance has been well described in rice plant hoppers (Matsumura et al, 2008;Wang et al, 2008), peach potato aphids (Foster et al, 2008), and whiteflies . Neonicotinoid resistance is often the result of enhanced metabolism (Karunker et al, 2008;Nauen et al, 2008), but there are examples of reduced sensitivity to neonicotinoids at the target site.…”

Section: Target-based Neonicotinoid Resistance: a Structural Interprementioning

confidence: 99%

Diverse Actions and Target-Site Selectivity of Neonicotinoids: Structural Insights

Matsuda

Kanaoka²,

Akamatsu³

et al. 2009

Mol Pharmacol

116

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The nicotinic acetylcholine receptors (nAChRs) are targets for human and veterinary medicines as well as insecticides. Subtypeselectivity among the diverse nAChR family members is important for medicines targeting particular disorders, and pest-insect selectivity is essential for the development of safer, environmentally acceptable insecticides. Neonicotinoid insecticides selectively targeting insect nAChRs have important applications in crop protection and animal health. Members of this class exhibit strikingly diverse actions on their nAChR targets. Here we review the chemistry and diverse actions of neonicotinoids on insect and mammalian nAChRs. Electrophysiological studies on native nAChRs and on wild-type and mutagenized recombinant nAChRs have shown that basic residues particular to loop D of insect nAChRs are likely to interact electrostatically with the nitro group of neonicotinoids. In 2008, the crystal structures were published showing neonicotinoids docking into the acetylcholine binding site of molluscan acetylcholine binding proteins with homology to the ligand binding domain (LBD) of nAChRs. The crystal structures showed that 1) glutamine in loop D, corresponding to the basic residues of insect nAChRs, hydrogen bonds with the NO 2 group of imidacloprid and 2) neonicotinoid-unique stacking and CHbonds at the LBD. A neonicotinoid-resistant strain obtained by laboratory-screening has been found to result from target site mutations, and possible reasons for this are also suggested by the crystal structures. The prospects of designing neonicotinoids that are safe not only for mammals but also for beneficial insects such as honey bees (Apis mellifera) are discussed in terms of interactions with non-␣ nAChR subunits.

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Correlated responses to neonicotinoid insecticides in clones of the peach‐potato aphid, Myzus persicae (Hemiptera: Aphididae)

Cited by 51 publications

References 19 publications

Management of Severe Curly Top in Sugar Beet with Insecticides

Management of Severe Curly Top in Sugar Beet with Insecticides

Gene amplification and microsatellite polymorphism underlie a recent insect host shift

Diverse Actions and Target-Site Selectivity of Neonicotinoids: Structural Insights

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