Evidence map›Paper›PMID 30190478›Full record

ArticleNature communications2018

Nucleolar fibrillarin is an evolutionarily conserved regulator of bacterial pathogen resistance.

Varnesh Tiku, Chun Kew, Parul Mehrotra, Raja Ganesan, Nirmal Robinson, Adam Antebi

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. 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
2.5field-weighted citation impact, top 11% 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, 60 citations in OpenAlex.

  1. Review
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  10. 2'-RNA (New York, N.Y.) · 2024
    Review
  11. Advances in the structure and function of the nucleolar protein fibrillarin.Frontiers in cell and developmental biology · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Immunosenescence in Caenorhabditis elegans.Immunity & ageing : I & A · 2022
    Article
  18. Article
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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

6 authors at 3 institutions in 1 country.

Varnesh TikuMax Planck Institute for Biology of Ageing, Joseph Stelzmann Strasse 9b, 50931, Cologne, Germany.
Chun KewMax Planck Institute for Biology of Ageing, Joseph Stelzmann Strasse 9b, 50931, Cologne, Germany.
Parul MehrotraMax Planck Institute for Biology of Ageing, Joseph Stelzmann Strasse 9b, 50931, Cologne, Germany.
Raja GanesanCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50674, Cologne, Germany.
Nirmal RobinsonCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50674, Cologne, Germany. nirmal.robinson@uk-koeln.de.
Adam AntebiMax Planck Institute for Biology of Ageing, Joseph Stelzmann Strasse 9b, 50931, Cologne, Germany. Antebi@age.mpg.de.
Max Planck Institute for Biology of Ageing · DECologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate immunity is the first line of defense against infections. Pathways regulating innate responses can also modulate other processes, including stress resistance and longevity. Increasing evidence suggests a role for the nucleolus in regulating cellular processes implicated in health and disease. Here we show the highly conserved nucleolar protein, fibrillarin, is a vital factor regulating pathogen resistance. Fibrillarin knockdown enhances resistance in C. elegans against bacterial pathogens, higher levels of fibrillarin induce susceptibility to infection. Pathogenic infection reduces nucleolar size, ribsosomal RNA, and fibrillarin levels. Genetic epistasis reveals fibrillarin functions independently of the major innate immunity mediators, suggesting novel mechanisms of pathogen resistance. Bacterial infection also reduces nucleolar size and fibrillarin levels in mammalian cells. Fibrillarin knockdown prior to infection increases intracellular bacterial clearance, reduces inflammation, and enhances cell survival. Collectively, these findings reveal an evolutionarily conserved role of fibrillarin in infection resistance and suggest the nucleolus as a focal point in innate immune responses.

Indexed as

Disease ResistanceHost-Pathogen InteractionsAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCaenorhabditis elegans ProteinsCell NucleolusChromosomal Proteins, Non-HistoneEnterococcus faecalisEvolution, MolecularFemaleGene Knockdown TechniquesHeLa CellsHumansMice, Inbred C57BLMutationCaenorhabditis elegans ProteinsChromosomal Proteins, Non-Histonefib-1 protein, C elegansfibrillarin

Identifiers

PMID30190478
PMCPMC6127302
OpenAlexW2888815313

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.