The Toll pathway mediates Drosophila resilience to Aspergillus mycotoxins through specific Bomanins

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Abstract
Host defense against infections encompasses both resistance, which targets microorganisms for neutralization or elimination, and resilience/disease tolerance, which allows the host to withstand/tolerate pathogens and repair damages. In Drosophila, the Toll signaling pathway is thought to mediate resistance against fungal infections by regulating the secretion of antimicrobial peptides, potentially including Bomanins. We find that Aspergillus fumigatus kills Drosophila Toll pathway mutants without invasion because its dissemination is blocked by melanization, suggesting a role for Toll in host defense distinct from resistance. We report that mutants affecting the Toll pathway or the 55C Bomanin locus are susceptible to the injection of two Aspergillus mycotoxins, restrictocin and verruculogen. The vulnerability of 55C deletion mutants to these mycotoxins is rescued by the overexpression of Bomanins specific to each challenge. Mechanistically, flies in which BomS6 is expressed in the nervous system exhibit an enhanced recovery from the tremors induced by injected verruculogen and display improved survival. Thus, innate immunity also protects the host against the action of microbial toxins through secreted peptides and thereby increases its resilience to infection.
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Funding Information
  • Agence Nationale de la Recherche (ANR‐17‐CE12‐0025)
  • Association Platform BioPark of Archamps Research and Development Funds
  • Higher Education Discipline Innovation Project (D18010)
  • Deutsche Forschungsgemeinschaft (210879364)
  • Excellence Cluster Balance of the Microverse
  • Guangzhou Medical University
  • Open Project from State Key Laboratory of Respiratory Diseases, China
  • China High‐end Foreign Talent Program
  • Sino‐Foreign Cooperative Graduate Education Project of Guangzhou Medical University
  • International Training Plan for Young Outstanding Scientific Research Talents of Guangdong Province

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