ArticlePLoS pathogens2023
The genetic basis of variation in immune defense against Lysinibacillus fusiformis infection in Drosophila melanogaster.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The genomic resource of Lysinibacillus fusiformis KBD-5, a biocontrol agent with antifungal activity against Botrytis cinerea.BMC genomics · 2026Article
- Atg8 orchestrates stress-responsive chromatin programs across immunity and metabolism.bioRxiv : the preprint server for biology · 2026Article
- Distinct Bomanins at the Drosophila 55C locus function in resistance and resilience to infections.EMBO reports · 2026Article
- Article
- Crop diversity induces trade-offs in microbial biopesticide susceptibility that could delay pest resistance evolution.PLoS pathogens · 2025Article
- Latitudinal Clines in Climate and Sleep Patterns Shape Disease Outcomes inEcology and evolution · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The genetic causes of phenotypic variation often differ depending on the population examined, particularly if the populations were founded by relatively small numbers of genotypes. Similarly, the genetic causes of phenotypic variation among similar traits (resistance to different xenobiotic compounds or pathogens) may also be completely different or only partially overlapping. Differences in genetic causes for variation in the same trait among populations suggests context dependence for how selection acts on those traits. Similarities in the genetic causes of variation for different traits, on the other hand, suggests pleiotropy which would also influence how natural selection shapes variation in a trait. We characterized immune defense against a natural Drosophila pathogen, the Gram-positive bacterium Lysinibacillus fusiformis, in three different populations and found almost no overlap in the genetic architecture of variation in survival post infection. However, when comparing our results to a similar experiment with the fungal pathogen, B. bassiana, we found a convincing shared QTL peak for both pathogens. This peak contains the Bomanin cluster of Drosophila immune effectors. Loss of function mutants and RNAi knockdown experiments confirms a role of some of these genes in immune defense against both pathogens. This suggests that natural selection may act on the entire cluster of Bomanin genes (and the linked region under the QTL) or specific peptides for specific pathogens.
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Registered trials
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 Socratic graph.