Evidence map›Paper›PMID 22212386›Full record

ArticleCellular microbiology2012

Autophagy is a cell death mechanism in Toxoplasma gondii.

Debasish Ghosh, Julia L Walton, Paul D Roepe, Anthony P Sinai

Abstract read
In one paragraph

Article in Cellular microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

69 citing papers in PubMed, 105 citations in OpenAlex.

  1. Review
  2. bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Elucidating the Role ofBiomolecules · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Detailing organelle division and segregation inbioRxiv : the preprint server for biology · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Regulation of phosphoinositide metabolism in Apicomplexan parasites.Frontiers in cell and developmental biology · 2023
    Review
  16. Article
  17. Article
  18. The Toxoplasma plant-like vacuolar compartment (PLVAC).The Journal of eukaryotic microbiology · 2022
    Review
  19. Review
  20. Article

9 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

4 authors at 2 institutions in 1 country.

Debasish GhoshDepartment of Microbiology, Immunology and Molecular Genetics, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Julia L Walton
Paul D Roepe
Anthony P Sinai
University of Kentucky · USGeorgetown University · US

Funding

Blockade of host apoptosis by Toxoplasma gondiiR01AI049367 · NIAID · UNIVERSITY OF KENTUCKY · PI SINAI, ANTHONY P. · 2001 to 2010
$2.6M
THE PHYSIOLOGY OF DRUG RESISTANT MALARIAR01AI045957 · NIAID · GEORGETOWN UNIVERSITY · PI ROEPE, PAUL D. · 2000 to 2009
$1.9M
NIAID NIH HHS R01 AI045957NIAID NIH HHS R01 AI049367NIAID NIH HHS R01AI049367
6 · The paper itself

Abstract

Nutrient sensing and the capacity to respond to starvation is tightly regulated as a means of cell survival. Among the features of the starvation response are induction of both translational repression and autophagy. Despite the fact that intracellular parasite like Toxoplasma gondii within a host cell predicted to be nutrient rich, they encode genes involved in both translational repression and autophagy. We therefore examined the consequence of starvation, a classic trigger of autophagy, on intracellular parasites. As expected, starvation results in the activation of the translational repression system as evidenced by elevation of phosphorylated TgIF2α (TgIF2α-P). Surprisingly, we also observe a rapid and selective fragmentation of the single parasite mitochondrion that leads irreversibly to parasite death. This profound effect was dependent primarily on the limitation of amino acids and involved signalling by the parasite TOR homologue. Notably, the effective blockade of mitochondrial fragmentation by the autophagy inhibitor 3-methyl adenine (3-MA) suggests an autophagic mechanism. In the absence of a documented apoptotic cascade in T. gondii, the data suggest that autophagy is the primary mechanism of programmed cell death in T. gondii and potentially other related parasites.

Indexed as

AutophagyAdenineAmino AcidsAnimalsCell SurvivalChlorocebus aethiopsCulture MediaEnergy MetabolismHost-Parasite InteractionsHumansMembrane Potential, MitochondrialMicroscopy, Electron, TransmissionMitochondriaProkaryotic Initiation Factor-2Protein BiosynthesisSignal Transduction3-methyladenineAdenineAmino AcidsCulture MediaProkaryotic Initiation Factor-2Sirolimus

Identifiers

PMID22212386
PMCPMC3302960
OpenAlexW1853875806

What OpenQuestion holds

Textmetadata
LicenceTDM
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.