Evidence map›Paper›PMID 28317932›Full record

ArticleScientific reports2017

Bacterial secretion system skews the fate of Legionella-containing vacuoles towards LC3-associated phagocytosis.

Andree Hubber, Tomoko Kubori, Cevayir Coban, Takeshi Matsuzawa, Michinaga Ogawa, Tsuyoshi Kawabata, Tamotsu Yoshimori, Hiroki Nagai

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. DRAM1 confers resistance toAutophagy reports · 2023
    Article
  5. Review
  6. Review
  7. LC3-Associated Phagocytosis in Bacterial Infection.Pathogens (Basel, Switzerland) · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Frontiers in cellular and infection microbiology · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Extracellular vesicles deliverEMBO reports · 2019
    Article
  20. LC3-associated phagocytosis at a glance.Journal of cell science · 2019
    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 at 3 institutions in 1 country.

Andree HubberResearch Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.
Tomoko KuboriResearch Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.
Cevayir CobanLaboratory of Malaria Immunology, Immunology Frontier Research Centre, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.
Takeshi MatsuzawaGraduate School of Life and Environmental Sciences, Osaka Prefecture University, Rinku Ohrai Kita 1-58, Izumisano, Osaka 598-8531, Japan.
Michinaga OgawaDepartment of Bacteriology I, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan.
Tsuyoshi KawabataDepartment of Genetics, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Tamotsu YoshimoriDepartment of Genetics, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Hiroki NagaiResearch Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.
Osaka University · JPNational Institute of Infectious Diseases · JPOsaka Prefecture University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The evolutionarily conserved processes of endosome-lysosome maturation and macroautophagy are established mechanisms that limit survival of intracellular bacteria. Similarly, another emerging mechanism is LC3-associated phagocytosis (LAP). Here we report that an intracellular vacuolar pathogen, Legionella dumoffii, is specifically targeted by LAP over classical endocytic maturation and macroautophagy pathways. Upon infection, the majority of L. dumoffii resides in ER-like vacuoles and replicate within this niche, which involves inhibition of classical endosomal maturation. The establishment of the replicative niche requires the bacterial Dot/Icm type IV secretion system (T4SS). Intriguingly, the remaining subset of L. dumoffii transiently acquires LC3 to L. dumoffii-containing vacuoles in a Dot/Icm T4SS-dependent manner. The LC3-decorated vacuoles are bound by an apparently undamaged single membrane, and fail to associate with the molecules implicated in selective autophagy, such as ubiquitin or adaptors. The process requires toll-like receptor 2, Rubicon, diacylglycerol signaling and downstream NADPH oxidases, whereas ULK1 kinase is dispensable. Together, we have discovered an intracellular pathogen, the survival of which in infected cells is limited predominantly by LAP. The results suggest that L. dumoffii is a valuable model organism for examining the mechanistic details of LAP, particularly induced by bacterial infection.

Indexed as

Bacterial Secretion SystemsPhagocytosisAnimalsAutophagyAutophagy-Related Protein-1 HomologBiomarkersDiglyceridesEndoplasmic ReticulumEndosomesHEK293 CellsHeLa CellsHumansIntracellular SpaceLegionellaLegionellosisMiceAutophagy-Related Protein-1 HomologBacterial Secretion SystemsBiomarkersDiglyceridesMap1lc3b protein, mouseMicrotubule-Associated ProteinsNADPH OxidasesToll-Like Receptor 2UbiquitinUlk1 protein, mouse

Identifiers

PMID28317932
PMCPMC5357938
OpenAlexW2598419231

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.