Evidence map›Paper›PMID 28103313›Full record

ArticlePLoS pathogens2017

Mycobacterium marinum Degrades Both Triacylglycerols and Phospholipids from Its Dictyostelium Host to Synthesise Its Own Triacylglycerols and Generate Lipid Inclusions.

Caroline Barisch, Thierry Soldati

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.8field-weighted citation impact, top 6% of its field
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

35 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Journal of bacteriology · 2025
    Review
  3. Frontiers in tuberculosis · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Frontiers in immunology · 2024
    Article
  9. Article
  10. Article
  11. The High Plasticity of NonpathogenicInternational journal of molecular sciences · 2022
    Article
  12. Review
  13. Review
  14. Article
  15. Disparate regulation of IMD signaling drives sex differences in infection pathology inProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  16. Review
  17. Mycobacterial fatty acid catabolism is repressed by FdmR to sustain lipogenesis and virulence.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Metabolic Versatility ofMetabolites · 2021
    Review
  19. Review
  20. Article
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

2 authors at 1 institution in 1 country.

Caroline BarischDepartment of Biochemistry, Science II, University of Geneva, 30 quai Ernest-Ansermet, Geneva, Switzerland.ORCID 0000-0002-1493-9006
Thierry SoldatiDepartment of Biochemistry, Science II, University of Geneva, 30 quai Ernest-Ansermet, Geneva, Switzerland.ORCID 0000-0002-2056-7931
University of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During a tuberculosis infection and inside lipid-laden foamy macrophages, fatty acids (FAs) and sterols are the major energy and carbon source for Mycobacterium tuberculosis. Mycobacteria can be found both inside a vacuole and the cytosol, but how this impacts their access to lipids is not well appreciated. Lipid droplets (LDs) store FAs in form of triacylglycerols (TAGs) and are energy reservoirs of prokaryotes and eukaryotes. Using the Dictyostelium discoideum/Mycobacterium marinum infection model we showed that M. marinum accesses host LDs to build up its own intracytosolic lipid inclusions (ILIs). Here, we show that host LDs aggregate at regions of the bacteria that become exposed to the cytosol, and appear to coalesce on their hydrophobic surface leading to a transfer of diacylglycerol O-acyltransferase 2 (Dgat2)-GFP onto the bacteria. Dictyostelium knockout mutants for both Dgat enzymes are unable to generate LDs. Instead, the excess of exogenous FAs is esterified predominantly into phospholipids, inducing uncontrolled proliferation of the endoplasmic reticulum (ER). Strikingly, in absence of host LDs, M. marinum alternatively exploits these phospholipids, resulting in rapid reversal of ER-proliferation. In addition, the bacteria are unable to restrict their acquisition of lipids from the dgat1&2 double knockout leading to vast accumulation of ILIs. Recent data indicate that the presence of ILIs is one of the characteristics of dormant mycobacteria. During Dictyostelium infection, ILI formation in M. marinum is not accompanied by a significant change in intracellular growth and a reduction in metabolic activity, thus providing evidence that storage of neutral lipids does not necessarily induce dormancy.

Indexed as

Chromatography, Thin LayerDictyosteliumFluorescent Antibody TechniqueHost-Pathogen InteractionsInclusion BodiesMicroscopy, Electron, TransmissionMycobacterium Infections, NontuberculousMycobacterium marinumPhospholipidsTriglyceridesPhospholipidsTriglycerides

Identifiers

PMID28103313
PMCPMC5245797
OpenAlexW2574541252

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.