Evidence map›Paper›PMID 40911634›Full record

ArticlePLoS pathogens2025

Genome-wide phenotypic insights into mycobacterial virulence using Drosophila melanogaster.

Niruja Sivakumar, Esther Fuentes, Linn-Karina Selvik, Marta Arch, Christina Gabrielsen Ås, Pere-Joan Cardona, Thomas R Ioerger, Marte Singsås Dragset

Abstract read
In one paragraph

Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Massively parallel mutant selection identifies genetic determinants ofbioRxiv : the preprint server for biology · 2023
    Article
  4. Genes · 2022
    Review
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

8 authors.

Niruja SivakumarCentre for Molecular Inflammation Research (CEMIR), Norwegian University of, Science and Technology (NTNU), Trondheim, Norway.
Esther FuentesTuberculosis Research Unit, Germans Trias i Pujol Research Institute (IGTP), Badalona, Spain.
Linn-Karina SelvikCentre for Molecular Inflammation Research (CEMIR), Norwegian University of, Science and Technology (NTNU), Trondheim, Norway.
Marta ArchTuberculosis Research Unit, Germans Trias i Pujol Research Institute (IGTP), Badalona, Spain.
Christina Gabrielsen ÅsDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
Pere-Joan CardonaTuberculosis Research Unit, Germans Trias i Pujol Research Institute (IGTP), Badalona, Spain.
Thomas R IoergerDepartment of Computer Science and Engineering, Texas A&M University, College Station, Texas, United States of America.
Marte Singsås DragsetCentre for Molecular Inflammation Research (CEMIR), Norwegian University of, Science and Technology (NTNU), Trondheim, Norway.ORCID 0000-0003-1546-4329

Funding

European Society of Clinical Microbiology and Infectious Diseases (ESCMID)Research Council of NorwaySpanish Government-FEDER
6 · The paper itself

Abstract

Drosophila melanogaster (Drosophila) is one of the most extensively studied animal models we have, with a broad, advanced, and organized research community. Yet, Drosophila has barely been exploited to understand the underlying mechanisms of mycobacterial infections, which cause some of the deadliest infectious diseases humans are currently battling. Here, we identified mycobacterial genes required for the pathogen's growth during Drosophila infection. Using Mycobacterium marinum (Mmar) to model mycobacterial pathogens, we first validated that an established mycobacterial virulence factor, EccB1 of the ESX-1 Type VII secretion system, is required for Mmar growth within the flies. Subsequently, we identified Mmar virulence genes in Drosophila in a high-throughput genome-wide phenotypic manner using transposon insertion sequencing. Of the 181 identified virulence genes, the vast majority (91%) had orthologs in the tuberculosis-causing M. tuberculosis (Mtb), suggesting that the encoded virulence mechanisms may be conserved across Mmar and Mtb species. By studying one of the identified genes in more depth, the putative ATP-binding protein ABC transporter encoded by mmar_1660, we found that both the Mmar gene and its Mtb ortholog (rv3041c) were required for virulence in human macrophages as well. We pinpointed the probable virulence mechanism of the genes to their requirements for growth during iron limitation, a condition met by mycobacteria during host infection. Together, our results bring forward Drosophila as a promising host model to study and identify mycobacterial virulence factors, providing insights that may transfer to Mtb human infection.

Indexed as

Drosophila melanogasterMycobacterium Infections, NontuberculousMycobacterium marinumVirulence FactorsAnimalsBacterial ProteinsDisease Models, AnimalGenome, BacterialHumansMycobacterium tuberculosisPhenotypeVirulenceBacterial ProteinsVirulence Factors

Identifiers

PMID40911634
PMCPMC12425279

What Socratic holds

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LicenceCC BY
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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 Socratic graph.