Evidence map›Paper›PMID 18245331›Full record

ArticleGenetics2008

Identification of Drosophila mutants altering defense of and endurance to Listeria monocytogenes infection.

Janelle S Ayres, Nancy Freitag, David S Schneider

Abstract read
In one paragraph

Article in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

87 citing papers in PubMed.

  1. Article
  2. Review
  3. Parasite defense covaries with reproductive timing, not with resistance.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Listeria monocytogenes: from a saprophytic to a cytosolic virulent pathogen.World journal of microbiology & biotechnology · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Autophagy induced by taurolidine protects against polymicrobial sepsis by promoting both host resistance and disease tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  20. Review

27 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Janelle S AyresDepartment of Microbiology and Immunology, University of Illinois, Chicago, Illinois 60612, USA.
Nancy Freitag
David S Schneider

Funding

MOLECULAR BASIS OF HOST-PARASITE INTERACTIONT32AI007328 · NIAID · STANFORD UNIVERSITY · PI JUSTIN L SONNENBURG · 1987 to 2026
$11.9M
Using Drosphila Macrophages to Study Innate ImmunityR01AI053080 · NIAID · STANFORD UNIVERSITY · PI SCHNEIDER, DAVID S · 2003 to 2007
$2.0M
Host-pathogen Genetics Using Listeria and DrosophilaR01AI055651 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FREITAG, NANCY ELIZABETH · 2004 to 2008
$1.6M
NIAID NIH HHS AI055651NIAID NIH HHS R01 AI053080-01NIAID NIH HHS T32 AI007328
6 · The paper itself

Abstract

We extended the use of Drosophila beyond being a model for signaling pathways required for pattern recognition immune signaling and show that the fly can be used to identify genes required for pathogenesis and host-pathogen interactions. We performed a forward genetic screen to identify Drosophila mutations altering sensitivity to the intracellular pathogen Listeria monocytogenes. We recovered 18 mutants with increased susceptibility to infection, none of which were previously shown to function in a Drosophila immune response. Using secondary screens, we divided these mutants into two groups: In the first group, mutants have reduced endurance to infections but show no change in bacterial growth. This is a new fly immunity phenotype that is not commonly studied. In the second group, mutants have a typical defense defect in which bacterial growth is increased and survival is decreased. By further challenging mutant flies with L. monocytogenes mutants, we identified subgroups of fly mutants that affect specific stages of the L. monocytogenes life cycle, exit from the vacuole, or actin-based movement. There is no overlap between our genes and the hundreds of genes identified in Drosophila S2 cells fighting L. monocytogenes infection, using genomewide RNAi screens in vitro. By using a whole-animal model and screening for host survival, we revealed genes involved in physiologies different from those that were found in previous screens, which all had defects in defensive immune signaling.

Indexed as

AnimalsDrosophila melanogasterGenes, InsectListeria monocytogenesListeriosisMutationPhenotypeRNA-Binding ProteinsRNA Processing, Post-TranscriptionalSalmonella typhimuriumStaphylococcus aureusSurvival AnalysisUbiquitinationRNA-Binding Proteins

Identifiers

PMID18245331
PMCPMC2278058

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.