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Gene amplification and microsatellite polymorphism underlie a recent insect host shift.

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A specific gene, cytochrome P450 (CYP6CY3), allows aphids to detoxify nicotine, enabling adaptation to tobacco plants. This adaptation also confers resistance to neonicotinoid insecticides, driving insect evolution.

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Area of Science:

  • Molecular biology
  • Evolutionary biology
  • Entomology

Background:

  • Host plant shifts in insects can lead to speciation and agricultural pest issues.
  • Tobacco-adapted aphids (Myzus persicae nicotianae) exhibit reduced nicotine sensitivity and neonicotinoid resistance.

Purpose of the Study:

  • To investigate the molecular mechanisms behind the adaptation of Myzus persicae to tobacco.
  • To understand how this adaptation confers resistance to neonicotinoid insecticides.

Main Methods:

  • Quantified CYP6CY3 expression in tobacco-adapted vs. non-adapted aphids.
  • Assessed in vitro metabolism of nicotine and neonicotinoids by CYP6CY3.
  • Generated transgenic Drosophila to test in vivo resistance conferred by CYP6CY3.
  • Analyzed promoter regions and gene copy numbers for CYP6CY3.

Main Results:

  • Constitutive overexpression of CYP6CY3 in tobacco-adapted aphids correlates with nicotine tolerance.
  • CYP6CY3 efficiently metabolizes nicotine and neonicotinoids, conferring resistance in vitro and in vivo.
  • CYP6CY3 overexpression is driven by microsatellite expansion and gene amplification (up to 100 copies).

Conclusions:

  • CYP6CY3 overexpression was a prerequisite for the Myzus persicae host shift to tobacco.
  • Gene amplification and microsatellite polymorphism are key evolutionary drivers of insect host adaptation.