Evidence map›Paper›PMID 24466199›Full record

ArticlePloS one2014

The E2-like conjugation enzyme Atg3 promotes binding of IRG and Gbp proteins to Chlamydia- and Toxoplasma-containing vacuoles and host resistance.

Arun K Haldar, Anthony S Piro, Danielle M Pilla, Masahiro Yamamoto, Jörn Coers

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 2 pooled it
6.8field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 89 citations in OpenAlex.

  1. Guideline
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  13. The role of SIRT1 in the process ofFrontiers in microbiology · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. Binding Features and Functions of ATG3.Frontiers in cell and developmental biology · 2021
    Review
  18. Interferons: Tug of War Between Bacteria and Their Host.Frontiers in cellular and infection microbiology · 2021
    Review
  19. Article
  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

5 authors at 3 institutions in 2 countries.

Arun K HaldarDepartments of Molecular Genetics and Microbiology and Immunology, Duke University Medical Center, Durham, NC, United States of America.
Anthony S PiroDepartments of Molecular Genetics and Microbiology and Immunology, Duke University Medical Center, Durham, NC, United States of America.
Danielle M PillaDepartments of Molecular Genetics and Microbiology and Immunology, Duke University Medical Center, Durham, NC, United States of America.
Masahiro YamamotoDepartment of Microbiology and Immunology, Osaka University, Osaka, Japan.
Jörn CoersDepartments of Molecular Genetics and Microbiology and Immunology, Duke University Medical Center, Durham, NC, United States of America.
Duke Medical Center · USDuke University Hospital · USOsaka University · JP

Funding

IRGM-driven host responses to Chlamydia trachomatis infectionsR01AI103197 · NIAID · DUKE UNIVERSITY · PI COERS, JOERN · 2013 to 2023
$4.2M
Interferon-inducible cell-intrinsic host defense against Chlamydia trachomatisR37AI103197 · NIAID · DUKE UNIVERSITY · PI Jorn Coers · 2024 to 2026
$1.6M
NIAID NIH HHS AI103197NIAID NIH HHS R01 AI103197NIAID NIH HHS R37 AI103197
6 · The paper itself

Abstract

Cell-autonomous immunity to the bacterial pathogen Chlamydia trachomatis and the protozoan pathogen Toxoplasma gondii is controlled by two families of Interferon (IFN)-inducible GTPases: Immunity Related GTPases (IRGs) and Guanylate binding proteins (Gbps). Members of these two GTPase families associate with pathogen-containing vacuoles (PVs) and solicit antimicrobial resistance pathways specifically to the intracellular site of infection. The proper delivery of IRG and Gbp proteins to PVs requires the autophagy factor Atg5. Atg5 is part of a protein complex that facilitates the transfer of the ubiquitin-like protein Atg8 from the E2-like conjugation enzyme Atg3 to the lipid phosphatidylethanolamine. Here, we show that Atg3 expression, similar to Atg5 expression, is required for IRG and Gbp proteins to dock to PVs. We further demonstrate that expression of a dominant-active, GTP-locked IRG protein variant rescues the PV targeting defect of Atg3- and Atg5-deficient cells, suggesting a possible role for Atg proteins in the activation of IRG proteins. Lastly, we show that IFN-induced cell-autonomous resistance to C. trachomatis infections in mouse cells depends not only on Atg5 and IRG proteins, as previously demonstrated, but also requires the expression of Atg3 and Gbp proteins. These findings provide a foundation for a better understanding of IRG- and Gbp-dependent cell-autonomous resistance and its regulation by Atg proteins.

Indexed as

Disease ResistanceImmunityAnimalsAutophagy-Related Protein 5Autophagy-Related ProteinsChlamydia InfectionsChlamydia trachomatisChromosomes, MammalianGTP-Binding ProteinsGuanosine TriphosphateInclusion BodiesInterferon-gammaMiceMicrotubule-Associated ProteinsMutant ProteinsProtein BindingAtg3 protein, mouseAtg5 protein, mouseAutophagy-Related Protein 5Autophagy-Related ProteinsGTP-Binding ProteinsGuanosine TriphosphateInterferon-gammaMicrotubule-Associated ProteinsMutant ProteinsUbiquitin-Conjugating Enzymes

Identifiers

PMID24466199
PMCPMC3895038
OpenAlexW1992306174

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.