ArticleeLife2016
Gustatory-mediated avoidance of bacterial lipopolysaccharides via TRPA1 activation in Drosophila.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed.
- Uracil-driven ROS signaling and larval TrpA1-B neuron activation are required for priming the adult Drosophila gustatory response to bacteria.PLoS biology · 2026Article
- Multisensory pathogen detection drives rapid escape and shapes host-microbe interactions in Drosophila larvae.PLoS pathogens · 2026Article
- Bidirectional crosstalk between TRP channels and Toll-like receptors in inflammation and host defense.Journal of neuroinflammation · 2026Review
- Article
- Evolution of resistance and disease tolerance mechanisms to oral bacterial infection inOpen biology · 2025Article
- Harnessing Insect Chemosensory and Mechanosensory Receptors Involved in Feeding for Precision Pest Management.Life (Basel, Switzerland) · 2025Review
- Cell wall components of gut commensal bacteria stimulate peritrophic matrix formation in malaria vector mosquitoes through activation of the IMD pathway.PLoS biology · 2025Article
- Genetic Variation in Trophic Avoidance Behaviour Shows Fruit Flies are Generally Attracted to Bacterial Substrates.Ecology and evolution · 2024Article
- Article
- Larval microbiota primes the Drosophila adult gustatory response.Nature communications · 2024Article
- Tastant-receptor interactions: insights from the fruit fly.Frontiers in nutrition · 2024Review
- Lipopolysaccharide-Induced TRPA1 Upregulation in Trigeminal Neurons is Dependent on TLR4 and Vesicular Exocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Article
- The PhytopathogenPathogens (Basel, Switzerland) · 2023Article
- Enteric bacterial infection in Drosophila induces whole-body alterations in metabolic gene expression independently of the immune deficiency signaling pathway.G3 (Bethesda, Md.) · 2022Article
- Bacteria-Derived Peptidoglycan Triggers a Noncanonical Nuclear Factor-κB-Dependent Response inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Mutualism promotes insect fitness by fungal nutrient compensation and facilitates fungus propagation by mediating insect oviposition preference.The ISME journal · 2022Article
- Mutations ofInternational journal of molecular sciences · 2022Article
- Salmonella enterica changes Macrosteles quadrilineatus feeding behaviors resulting in altered S. enterica distribution on leaves and increased populations.Scientific reports · 2022Article
- The gut efflux pump MRP-1 exports oxidized glutathione as a danger signal that stimulates behavioral immunity and aversive learning.Communications biology · 2022Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Detecting pathogens and mounting immune responses upon infection is crucial for animal health. However, these responses come at a high metabolic price (McKean and Lazzaro, 2011, Kominsky et al., 2010), and avoiding pathogens before infection may be advantageous. The bacterial endotoxins lipopolysaccharides (LPS) are important immune system infection cues (Abbas et al., 2014), but it remains unknown whether animals possess sensory mechanisms to detect them prior to infection. Here we show that Drosophila melanogaster display strong aversive responses to LPS and that gustatory neurons expressing Gr66a bitter receptors mediate avoidance of LPS in feeding and egg laying assays. We found the expression of the chemosensory cation channel dTRPA1 in these cells to be necessary and sufficient for LPS avoidance. Furthermore, LPS stimulates Drosophila neurons in a TRPA1-dependent manner and activates exogenous dTRPA1 channels in human cells. Our findings demonstrate that flies detect bacterial endotoxins via a gustatory pathway through TRPA1 activation as conserved molecular mechanism.
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