Evidence map›Paper›PMID 16983090›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Autophagy-mediated reentry of Francisella tularensis into the endocytic compartment after cytoplasmic replication.

Claire Checroun, Tara D Wehrly, Elizabeth R Fischer, Stanley F Hayes, Jean Celli

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 217 papers.

0numbers the graph read from it
0cells of the map it votes in
217citing papers in PubMed
17.3field-weighted citation impact, top 1% 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

217 citing papers in PubMed, 341 citations in OpenAlex.

  1. Article
  2. Article
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  9. Article
  10. Breaking the cellular defense: the role of autophagy evasion inFrontiers in cellular and infection microbiology · 2024
    Article
  11. Review
  12. Intracellular Experimental Evolution ofACS infectious diseases · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Recruitment of LC3 byFrontiers in cellular and infection microbiology · 2022
    Article

157 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

5 authors at 2 institutions in 1 country.

Claire ChecrounTularemia Pathogenesis Section, Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South Fourth Street, Hamilton, MT 59840, USA.
Tara D Wehrly
Elizabeth R Fischer
Stanley F Hayes
Jean Celli
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Molecular Basis of Francisella tularensis-Macrophage InteractionsZIAAI000953 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CELLI, JEAN · 2009 to 2013
$5.0M
Molecular Basis of Francisella tularensis-Macrophage InteractionsZ01AI000953 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI CELLI, JEAN · 2005 to 2008
$2.0M
Intramural NIH HHS
6 · The paper itself

Abstract

Intracellular bacterial pathogens evade the bactericidal functions of mammalian cells by physical escape from their phagosome and replication into the cytoplasm or through the modulation of phagosome maturation and biogenesis of a membrane-bound replicative organelle. Here, we detail in murine primary macrophages the intracellular life cycle of Francisella tularensis, a highly infectious bacterium that survives and replicates within mammalian cells. After transient interactions with the endocytic pathway, bacteria escaped from their phagosome by 1 h after infection and underwent replication in the cytoplasm from 4 to 20 h after infection. Unexpectedly, the majority of bacteria were subsequently found to be enclosed within large, juxtanuclear, LAMP-1-positive vacuoles called Francisella-containing vacuoles (FCVs). FCV formation required intracytoplasmic replication of bacteria. Using electron and fluorescence microscopy, we observed that the FCVs contained morphologically intact bacteria, despite fusing with lysosomes. FCVs are multimembranous structures that accumulate monodansylcadaverine and display the autophagy-specific protein LC3 on their membrane. Formation of FCVs was significantly inhibited by 3-methyladenine, confirming a role for the autophagic pathway in the biogenesis of these organelles. Taken together, our results demonstrate that, via autophagy, F. tularensis reenters the endocytic pathway after cytoplasmic replication, a process thus far undescribed for intracellular pathogens.

Indexed as

DNA ReplicationAnimalsAutophagyBacterial VaccinesCell MembraneCells, CulturedEndocytosisFemaleFlow CytometryFrancisella tularensisLysosomesMacrophagesMiceMice, Inbred C57BLPhagosomesVacuolesBacterial Vaccines

Identifiers

PMID16983090
PMCPMC1600002
OpenAlexW1972506258

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.