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Is the CncC/Keap1 complex a major factor in conferring pesticide resistance in arthropods? - A critical review

  • Writer: Angeliki Milioti
    Angeliki Milioti
  • Jan 13
  • 1 min read

Abstract


The CncC/Keap1 signalling pathway regulates antioxidant and detoxification gene expression in arthropods and is frequently associated with metabolic insecticide resistance. This review critically assesses evidence for its role in resistance phenotypes across key pest species. Although overactivation of CncC/Keap1 correlates with increased detoxification enzyme expression and pesticide tolerance, causal mutations in the coding or regulatory regions of CncC, Keap1, or Maf remain unidentified. We evaluate the evidence supporting the role of CncC/Keap1 in pesticide resistance in insects and mites and report the latest advancements in our understanding of this system in arthropods. We further highlight the need for unbiased genetic mapping and reverse genetic approaches to resolve the mechanisms of constitutive CncC activation in resistant populations. Understanding these mechanisms is crucial for elucidating the origins of metabolic resistance and developing sustainable pest management strategies.


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Funded by the European Union. Views and opinions expressed are however those of the author(s) only and do not necessarily reflect those of the European Union or the European Research Executive Agency (REA). Neither the European Union nor the granting authority can be held responsible for them.

This work also received funding from UK Research and Innovation (UKRI) under the UK government’s Horizon Europe funding Guarantee, grant number 10091427.

This work was supported by the Government of Canada through the Genomic Applications Partnership Program (GAPP) (OGI-229).

Project coordination

Prof. John Vontas

vontas@imbb.forth.gr

Foundation for Research and Technology-Hellas (FORTH)

Project communication

MSc Angeliki Milioti

angeliki@smartagrohub.gr

Smart Agro Hub

Project Framework

This project has received funding from the European Union’s Horizon Europe research and innovation programme under grant agreement 101136611. Funded by the European Union. Views and opinions expressed are however those of the author(s) only and do not necessarily reflect those of the European Union or the European Research Executive Agency (REA). Neither the European Union nor the granting authority can be held responsible for them.

This work also received funding from UK Research and Innovation (UKRI) under the UK government’s Horizon Europe funding Guarantee, grant number 10091427.

This work was also supported by the Government of Canada through the Genomic Applications Partnership Program (GAPP) (OGI-229).

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