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Complexin in ivermectin resistance in body lice
Nadia Amanzougaghene1, Florence Fenollar2, Claude Nappez2
1Aix Marseille Univ, IRD, APHM, MEPHI, IHU-Méditerranée Infection, Marseille, France.
Plos Genetics
|August 7, 2018
Summary
Ivermectin resistance in body lice is not due to target-site mutations. Instead, reduced expression of the neuronal protein complexin, caused by a gene mutation, significantly contributes to ivermectin resistance.
Area of Science:
- Entomology
- Molecular Biology
- Parasitology
Background:
- Ivermectin is a crucial pediculicide, but resistance is emerging.
- Field-evolved ivermectin resistance in body lice necessitates understanding resistance mechanisms.
Purpose of the Study:
- Investigate mechanisms of ivermectin resistance in body lice.
- Identify genetic and proteomic factors contributing to ivermectin resistance.
Main Methods:
- Analyzed mutations in the ivermectin target site (GluCl).
- Performed proteomic analysis on susceptible and resistant body lice.
- Utilized qRT-PCR to correlate mRNA and protein levels.
- Confirmed complexin's role using RNA interference.
Main Results:
- No non-silent mutations were found in the GluCl target site.
- Proteomic analysis revealed 22 differentially expressed proteins, with complexin significantly downregulated.
- A nonsense mutation in complexin was identified, potentially causing its reduced expression.
- Knocking down complexin expression induced ivermectin resistance in susceptible lice.
Conclusions:
- Complexin plays a significant role in ivermectin resistance in body lice.
- This study provides the first evidence linking complexin to insecticide resistance.
- Mechanisms of ivermectin resistance involve complexin downregulation, not target-site mutations.
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