Evidence map›Paper›PMID 24068924›Full record

ArticlePLoS pathogens2013

Activation of Ran GTPase by a Legionella effector promotes microtubule polymerization, pathogen vacuole motility and infection.

Eva Rothmeier, Gudrun Pfaffinger, Christine Hoffmann, Christopher F Harrison, Heinrich Grabmayr, Urska Repnik, Mandy Hannemann, Stefan Wölke, Andreas Bausch, Gareth Griffiths and 3 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
7.8field-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

56 citing papers in PubMed, 104 citations in OpenAlex.

  1. Life science alliance · 2026
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  4. ThemSphere · 2025
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  5. Journal of bacteriology · 2024
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  10. Manipulating cell motility byJournal of translational internal medicine · 2023
    Article
  11. Review
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  13. Review
  14. Article
  15. Article
  16. eLife · 2022
    Article
  17. Article
  18. Article
  19. Evolution and Adaptation ofBiomolecules · 2021
    Review
  20. Frontiers in cell and developmental biology · 2021
    Review
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

13 authors at 4 institutions in 2 countries.

Eva RothmeierMax von Pettenkofer-Institute, Department of Medicine, Ludwig-Maximilians Universität München, München, Germany.
Gudrun Pfaffinger
Christine Hoffmann
Christopher F Harrison
Heinrich Grabmayr
Urska Repnik
Mandy Hannemann
Stefan Wölke
Andreas Bausch
Gareth Griffiths
Annette Müller-Taubenberger
Aymelt Itzen
Hubert Hilbi
Ludwig-Maximilians-Universität München · DETechnical University of Munich · DEUniversity of Oslo · NOCenter for Integrated Protein Science Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The causative agent of Legionnaires' disease, Legionella pneumophila, uses the Icm/Dot type IV secretion system (T4SS) to form in phagocytes a distinct "Legionella-containing vacuole" (LCV), which intercepts endosomal and secretory vesicle trafficking. Proteomics revealed the presence of the small GTPase Ran and its effector RanBP1 on purified LCVs. Here we validate that Ran and RanBP1 localize to LCVs and promote intracellular growth of L. pneumophila. Moreover, the L. pneumophila protein LegG1, which contains putative RCC1 Ran guanine nucleotide exchange factor (GEF) domains, accumulates on LCVs in an Icm/Dot-dependent manner. L. pneumophila wild-type bacteria, but not strains lacking LegG1 or a functional Icm/Dot T4SS, activate Ran on LCVs, while purified LegG1 produces active Ran(GTP) in cell lysates. L. pneumophila lacking legG1 is compromised for intracellular growth in macrophages and amoebae, yet is as cytotoxic as the wild-type strain. A downstream effect of LegG1 is to stabilize microtubules, as revealed by conventional and stimulated emission depletion (STED) fluorescence microscopy, subcellular fractionation and Western blot, or by microbial microinjection through the T3SS of a Yersinia strain lacking endogenous effectors. Real-time fluorescence imaging indicates that LCVs harboring wild-type L. pneumophila rapidly move along microtubules, while LCVs harboring ΔlegG1 mutant bacteria are stalled. Together, our results demonstrate that Ran activation and RanBP1 promote LCV formation, and the Icm/Dot substrate LegG1 functions as a bacterial Ran activator, which localizes to LCVs and promotes microtubule stabilization, LCV motility as well as intracellular replication of L. pneumophila.

Indexed as

AnimalsBacterial ProteinsCell LineEnzyme ActivationGene SilencingGTPase-Activating ProteinsHumansLegionella pneumophilaLegionnaires' DiseaseMacrophagesMiceMicrotubule ProteinsMicrotubulesMutationPhagocytosisPhagosomesBacterial ProteinsGTPase-Activating ProteinsMicrotubule ProteinsRangap1 protein, mouseran GTP-Binding ProteinRan protein, mouse

Identifiers

PMID24068924
PMCPMC3777869
OpenAlexW2059100138

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.