Evidence map›Paper›PMID 31327526›Full record

ArticleCell2019

A Bacterial Effector Reveals the V-ATPase-ATG16L1 Axis that Initiates Xenophagy.

Yue Xu, Ping Zhou, Sen Cheng, Qiuhe Lu, Kathrin Nowak, Ann-Katrin Hopp, Lin Li, Xuyan Shi, Zhiwei Zhou, Wenqing Gao and 6 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 241 papers.

0numbers the graph read from it
0cells of the map it votes in
241citing papers in PubMed
24.6field-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

241 citing papers in PubMed, 359 citations in OpenAlex.

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  17. Restricting intracellularAutophagy · 2026
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  18. Role of autophagy in antiviral innate immunity.Cellular & molecular biology letters · 2026
    Review
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181 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 2 countries.

Yue XuCollege of Biological Sciences, China Agricultural University, 100094 Beijing, China; National Institute of Biological Sciences, Beijing, 102206 Beijing, China.
Ping ZhouNational Institute of Biological Sciences, Beijing, 102206 Beijing, China.
Sen ChengInstitute of Analytical Chemistry & Synthetic and Functional Biomolecules Center, College of Chemistry and Molecular Engineering, Peking University, 100871 Beijing, China.
Qiuhe LuNational Institute of Biological Sciences, Beijing, 102206 Beijing, China.
Kathrin NowakDepartment of Molecular Mechanisms of Disease, University of Zurich, 8057 Zurich, Switzerland.
Ann-Katrin HoppDepartment of Molecular Mechanisms of Disease, University of Zurich, 8057 Zurich, Switzerland.
Lin LiNational Institute of Biological Sciences, Beijing, 102206 Beijing, China.
Xuyan ShiNational Institute of Biological Sciences, Beijing, 102206 Beijing, China.
Zhiwei ZhouNational Institute of Biological Sciences, Beijing, 102206 Beijing, China.
Wenqing GaoNational Institute of Biological Sciences, Beijing, 102206 Beijing, China.
Da LiNational Institute of Biological Sciences, Beijing, 102206 Beijing, China.
Huabin HeNational Institute of Biological Sciences, Beijing, 102206 Beijing, China.
Xiaoyun LiuInstitute of Analytical Chemistry & Synthetic and Functional Biomolecules Center, College of Chemistry and Molecular Engineering, Peking University, 100871 Beijing, China.
Jingjin DingNational Institute of Biological Sciences, Beijing, 102206 Beijing, China; National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101 Beijing, China.
Michael O HottigerDepartment of Molecular Mechanisms of Disease, University of Zurich, 8057 Zurich, Switzerland.
Feng ShaoNational Institute of Biological Sciences, Beijing, 102206 Beijing, China; Tsinghua Institute of Multidisciplinary Biomedical Research, Tsinghua University, 102206 Beijing, China. Electronic address: shaofeng@nibs.ac.cn.
National Institute of Biological Sciences, Beijing · CNUniversity of Zurich · CHPeking University · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antibacterial autophagy (xenophagy) is an important host defense, but how it is initiated is unclear. Here, we performed a bacterial transposon screen and identified a T3SS effector SopF that potently blocked Salmonella autophagy. SopF was a general xenophagy inhibitor without affecting canonical autophagy. S. Typhimurium ΔsopF resembled S. flexneri ΔvirAΔicsB with the majority of intracellular bacteria targeted by autophagy, permitting a CRISPR screen that identified host V-ATPase as an essential factor. Upon bacteria-caused vacuolar damage, the V-ATPase recruited ATG16L1 onto bacteria-containing vacuole, which was blocked by SopF. Mammalian ATG16L1 bears a WD40 domain required for interacting with the V-ATPase. Inhibiting autophagy by SopF promoted S. Typhimurium proliferation in vivo. SopF targeted Gln124 of ATP6V0C in the V-ATPase for ADP-ribosylation. Mutation of Gln124 also blocked xenophagy, but not canonical autophagy. Thus, the discovery of SopF reveals the V-ATPase-ATG16L1 axis that critically mediates autophagic recognition of intracellular pathogen.

Indexed as

MacroautophagyADP-RibosylationAutophagy-Related ProteinsBacterial ProteinsCRISPR-Cas SystemsGene EditingHeLa CellsHumansMicrotubule-Associated ProteinsProtein BindingSalmonellaType III Secretion SystemsVacuolar Proton-Translocating ATPasesVirulence FactorsATG16L1 protein, humanAutophagy-Related ProteinsBacterial ProteinsMAP1LC3A protein, humanMicrotubule-Associated ProteinsRB1CC1 protein, humanType III Secretion SystemsVacuolar Proton-Translocating ATPasesVirulence FactorsADP-ribosylationautophagybacteria-host interactioninnate immunitytype III secretion systemV-ATPasexenophagy

Identifiers

PMID31327526
OpenAlexW2961013416

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.