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Neonicotinoid insecticide interact with honeybee odorant-binding protein: Implication for olfactory dysfunction.

Hongliang Li1, Fan Wu2, Lei Zhao2

  • 1Zhejiang Provincial Key Laboratory of Biometrology and Inspection & Quarantine, College of Life Sciences, China Jiliang University, Hangzhou 310018, China; College of Animal Sciences, Zhejiang University, Hangzhou 310058, China.

International Journal of Biological Macromolecules
|August 31, 2015
PubMed
Summary
This summary is machine-generated.

Neonicotinoid imidacloprid disrupts bee olfaction by binding to the ASP2 protein, impairing their ability to detect floral scents. This interaction affects bee pollination crucial for agriculture.

Keywords:
Binding interactionImidaclopridMolecular dockingMultispectroscopyOdorant-binding proteinSite-directed mutagenesis

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Area of Science:

  • Environmental Science
  • Insect Biochemistry
  • Chemical Ecology

Background:

  • Bee population decline is a significant environmental concern.
  • Neonicotinoid insecticides are implicated in bee impairment.
  • The precise interaction of neonicotinoids with bee olfactory systems remains unclear.

Purpose of the Study:

  • To investigate the binding interaction between imidacloprid and the Apis cerana odorant-binding protein ASP2.
  • To elucidate the mechanism of neonicotinoid interaction with bee olfactory proteins.
  • To assess the impact of imidacloprid on bee olfactory function.

Main Methods:

  • Multispectroscopic methods (fluorescence, circular dichroism) were used to study imidacloprid-ASP2 binding.
  • Thermodynamic analysis determined the driving forces of the interaction.
  • Molecular docking and site-directed mutagenesis explored binding site interactions.
  • Binding affinity assays measured the effect of imidacloprid on ASP2's interaction with a floral volatile.

Main Results:

  • Imidacloprid binds to ASP2 via static quenching and alters its conformation.
  • Hydrophobic forces are the primary drivers of the imidacloprid-ASP2 interaction.
  • While docking suggested a hydrogen bond, mutagenesis indicated it's not the main binding force.
  • Sublethal imidacloprid doses reduced ASP2's affinity for the floral volatile β-ionone.

Conclusions:

  • Imidacloprid directly interacts with and alters the function of the bee olfactory protein ASP2.
  • This interaction, driven by hydrophobic forces, impairs the bee's ability to detect floral scents.
  • Findings provide insights into neonicotinoid effects on bee olfactory cognition and pollination.