Evidence map›Paper›PMID 26451915›Full record

ArticlePLoS pathogens2015

The Autophagy Receptor TAX1BP1 and the Molecular Motor Myosin VI Are Required for Clearance of Salmonella Typhimurium by Autophagy.

David A Tumbarello, Paul T Manna, Mark Allen, Mark Bycroft, Susan D Arden, John Kendrick-Jones, Folma Buss

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 132 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed, 4 pooled it
12.4field-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

132 citing papers in PubMed, 4 syntheses or guidelines pooled it, 206 citations in OpenAlex.

  1. Pooled it
  2. Guideline
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  11. UBE4B Mediates Mitophagy via NIPSNAP1 Ubiquitination and NDP52 Recruitment.International journal of molecular sciences · 2026
    Article
  12. Article
  13. Mechanistic insights into the iron-sulfur cluster-dependent interaction of the autophagy receptor NCOA4 with the E3 ligase HERC2.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  14. Review
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72 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

David A TumbarelloCambridge Institute for Medical Research, University of Cambridge, Cambridge, United Kingdom.
Paul T MannaCambridge Institute for Medical Research, University of Cambridge, Cambridge, United Kingdom.
Mark AllenMRC Laboratory of Molecular Biology, Cambridge, United Kingdom.
Mark BycroftMRC Laboratory of Molecular Biology, Cambridge, United Kingdom.
Susan D ArdenCambridge Institute for Medical Research, University of Cambridge, Cambridge, United Kingdom.
John Kendrick-JonesMRC Laboratory of Molecular Biology, Cambridge, United Kingdom.
Folma BussCambridge Institute for Medical Research, University of Cambridge, Cambridge, United Kingdom.
University of Cambridge · GBMRC Laboratory of Molecular Biology · GB

Funding

Medical Research Council MC_U105184323Medical Research Council MC_U105184326Medical Research Council MR/K000888/1Medical Research Council U105184325Wellcome Trust 086743Wellcome Trust 093026Wellcome Trust 100140
6 · The paper itself

Abstract

Autophagy plays a key role during Salmonella infection, by eliminating these pathogens following escape into the cytosol. In this process, selective autophagy receptors, including the myosin VI adaptor proteins optineurin and NDP52, have been shown to recognize cytosolic pathogens. Here, we demonstrate that myosin VI and TAX1BP1 are recruited to ubiquitylated Salmonella and play a key role in xenophagy. The absence of TAX1BP1 causes an accumulation of ubiquitin-positive Salmonella, whereas loss of myosin VI leads to an increase in ubiquitylated and LC3-positive bacteria. Our structural studies demonstrate that the ubiquitin-binding site of TAX1BP1 overlaps with the myosin VI binding site and point mutations in the TAX1BP1 zinc finger domains that affect ubiquitin binding also ablate binding to myosin VI. This mutually exclusive binding and the association of TAX1BP1 with LC3 on the outer limiting membrane of autophagosomes may suggest a molecular mechanism for recruitment of this motor to autophagosomes. The predominant role of TAX1BP1, a paralogue of NDP52, in xenophagy is supported by our evolutionary analysis, which demonstrates that functionally intact NDP52 is missing in Xenopus and mice, whereas TAX1BP1 is expressed in all vertebrates analysed. In summary, this work highlights the importance of TAX1BP1 as a novel autophagy receptor in myosin VI-mediated xenophagy. Our study identifies essential new machinery for the autophagy-dependent clearance of Salmonella typhimurium and suggests modulation of myosin VI motor activity as a potential therapeutic target in cellular immunity.

Indexed as

Salmonella typhimuriumAnimalsAutophagyBlotting, WesternCells, CulturedGene Knockdown TechniquesHeLa CellsHumansImmunoprecipitationIntracellular Signaling Peptides and ProteinsMagnetic Resonance SpectroscopyMiceMicroscopy, FluorescenceMolecular Sequence DataMyosin Heavy ChainsNeoplasm ProteinsIntracellular Signaling Peptides and ProteinsMyosin Heavy Chainsmyosin VINeoplasm ProteinsTAX1BP1 protein, human

Identifiers

PMID26451915
PMCPMC4599966
OpenAlexW4297810615

What OpenQuestion holds

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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.