ArticlePLoS pathogens2015
An effector Peptide family required for Drosophila toll-mediated immunity.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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Who cites it
87 citing papers in PubMed, 179 citations in OpenAlex.
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- A binary-distributed effector modulates fungal host preference for drosophilids by targeting a lineage-specific immune factor.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Functional characterization of Paillotin: an immune peptide regulated by the Immune deficiency (Imd) pathway with pathogen-specific roles inProceedings. Biological sciences · 2025Article
- Fruit flies exploit behavioral fever as a defense strategy against parasitic insects.Science advances · 2025Article
- Acquisition of daptomycin resistance in patients results in decreased virulence inInfection and immunity · 2025Article
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- Chronic bacterial infections exert metabolic costs in Drosophila melanogaster.The Journal of experimental biology · 2025Article
- An unusual Toll/MyD88-mediatedFly · 2024Article
- Glucocerebrosidase deficiency leads to neuropathology via cellular immune activation.PLoS genetics · 2024Article
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- The NFκB Dif is required for behavioral and molecular correlates of sleep homeostasis in Drosophila.Sleep · 2024Article
- MprF-mediated immune evasion is necessary for Lactiplantibacillus plantarum resilience in the Drosophila gut during inflammation.PLoS pathogens · 2024Article
27 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In Drosophila melanogaster, recognition of an invading pathogen activates the Toll or Imd signaling pathway, triggering robust upregulation of innate immune effectors. Although the mechanisms of pathogen recognition and signaling are now well understood, the functions of the immune-induced transcriptome and proteome remain much less well characterized. Through bioinformatic analysis of effector gene sequences, we have defined a family of twelve genes - the Bomanins (Boms) - that are specifically induced by Toll and that encode small, secreted peptides of unknown biochemical activity. Using targeted genome engineering, we have deleted ten of the twelve Bom genes. Remarkably, inactivating these ten genes decreases survival upon microbial infection to the same extent, and with the same specificity, as does eliminating Toll pathway function. Toll signaling, however, appears unaffected. Assaying bacterial load post-infection in wild-type and mutant flies, we provide evidence that the Boms are required for resistance to, rather than tolerance of, infection. In addition, by generating and assaying a deletion of a smaller subset of the Bom genes, we find that there is overlap in Bom activity toward particular pathogens. Together, these studies deepen our understanding of Toll-mediated immunity and provide a new in vivo model for exploration of the innate immune effector repertoire.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.