Evidence map›Paper›PMID 35046574›Full record

ArticleNature structural & molecular biology2022

ARF GTPases activate Salmonella effector SopF to ADP-ribosylate host V-ATPase and inhibit endomembrane damage-induced autophagy.

Yue Xu, Sen Cheng, Huan Zeng, Ping Zhou, Yan Ma, Lin Li, Xiaoyun Liu, Feng Shao, Jingjin Ding

Abstract read
PubMed Publisher
In one paragraph

Article in Nature structural & molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. ATG16L1 controls mammalian vacuolar proton ATPase.The Journal of cell biology · 2025
    Article
  10. Review
  11. cGAS-STING: mechanisms and therapeutic opportunities.Science China. Life sciences · 2025
    Review
  12. The interplay betweenCell insight · 2025
    Review
  13. Article
  14. STING-induced noncanonical autophagy regulates endolysosomal homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  15. Article
  16. Article
  17. Autophagy and Bacterial infections.Autophagy reports · 2025
    Review
  18. Molecular biology of the cell · 2025
    Article
  19. Review
  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

9 authors at 5 institutions in 1 country.

Yue XuNational Institute of Biological Sciences, Beijing, China.
Sen ChengInstitute of Analytical Chemistry and Synthetic and Functional Biomolecules Center, College of Chemistry and Molecular Engineering, Peking University, Beijing, China.
Huan ZengNational Institute of Biological Sciences, Beijing, China.
Ping ZhouNational Institute of Biological Sciences, Beijing, China.
Yan MaNational Institute of Biological Sciences, Beijing, China.
Lin LiNational Institute of Biological Sciences, Beijing, China.
Xiaoyun LiuInstitute of Analytical Chemistry and Synthetic and Functional Biomolecules Center, College of Chemistry and Molecular Engineering, Peking University, Beijing, China.ORCID http://orcid.org/0000-0001-7083-5263
Feng ShaoNational Institute of Biological Sciences, Beijing, China. shaofeng@nibs.ac.cn.ORCID http://orcid.org/0000-0002-9562-7791
Jingjin DingNational Institute of Biological Sciences, Beijing, China. jding@ibp.ac.cn.ORCID http://orcid.org/0000-0001-9941-7997
National Institute of Biological Sciences, Beijing · CNChinese Academy of Sciences · CNPeking University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Selective autophagy helps eukaryotes to cope with endogenous dangers or foreign invaders; its initiation often involves membrane damage. By studying a Salmonella effector SopF, we recently identified the vacuolar ATPase (V-ATPase)-ATG16L1 axis that initiates bacteria-induced autophagy. Here we show that SopF is an ADP-ribosyltransferase specifically modifying Gln124 of ATP6V0C in V-ATPase. We identify GTP-bound ADP-ribosylation factor (ARF) GTPases as a cofactor required for SopF functioning. Crystal structures of SopF-ARF1 complexes not only reveal structural basis of SopF ADP-ribosyltransferase activity but also a unique effector-binding mode adopted by ARF GTPases. Further, the N terminus of ARF1, although dispensable for high-affinity binding to SopF, is critical for activating SopF to modify ATP6V0C. Moreover, lysosome or Golgi damage-induced autophagic LC3 activation is inhibited by SopF or Q124A mutation of ATP6V0C, thus also mediated by the V-ATPase-ATG16L1 axis. In this process, the V-ATPase functions to sense membrane damages, which can be uncoupled from its proton-pumping activity.

Indexed as

AutophagyADP-Ribosylation FactorsBacterial ProteinsOrganellesProtein BindingSalmonellaVacuolar Proton-Translocating ATPasesADP-Ribosylation FactorsBacterial ProteinsVacuolar Proton-Translocating ATPases

Identifiers

PMID35046574
OpenAlexW4205992721

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.