Evidence map›Paper›PMID 26624285›Full record

ArticlePLoS genetics2015

The Ribosome Biogenesis Protein Nol9 Is Essential for Definitive Hematopoiesis and Pancreas Morphogenesis in Zebrafish.

Ewa Bielczyk-Maczyńska, Laure Lam Hung, Lauren Ferreira, Tobias Fleischmann, Félix Weis, Antonio Fernández-Pevida, Steven A Harvey, Neha Wali, Alan J Warren, Inês Barroso and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. A dual ribosomal system in the zebrafish soma and germline.bioRxiv : the preprint server for biology · 2024
    Article
  3. Article
  4. Review
  5. iScience · 2023
    Article
  6. Ribosome biogenesis and function in development and disease.Development (Cambridge, England) · 2023
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Loss of the homologous recombination geneProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  18. 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

12 authors at 4 institutions in 1 country.

Ewa Bielczyk-MaczyńskaDepartment of Haematology, University of Cambridge, Cambridge, United Kingdom.
Laure Lam HungWellcome Trust Sanger Institute, Genome Campus, Hinxton, Cambridge, United Kingdom.
Lauren FerreiraDepartment of Haematology, University of Cambridge, Cambridge, United Kingdom.
Tobias FleischmannDepartment of Haematology, University of Cambridge, Cambridge, United Kingdom.
Félix WeisDepartment of Haematology, University of Cambridge, Cambridge, United Kingdom.
Antonio Fernández-PevidaDepartment of Haematology, University of Cambridge, Cambridge, United Kingdom.
Steven A HarveyWellcome Trust Sanger Institute, Genome Campus, Hinxton, Cambridge, United Kingdom.
Neha WaliWellcome Trust Sanger Institute, Genome Campus, Hinxton, Cambridge, United Kingdom.
Alan J WarrenDepartment of Haematology, University of Cambridge, Cambridge, United Kingdom.
Inês BarrosoWellcome Trust Sanger Institute, Genome Campus, Hinxton, Cambridge, United Kingdom.
Derek L StempleWellcome Trust Sanger Institute, Genome Campus, Hinxton, Cambridge, United Kingdom.
Ana CvejicDepartment of Haematology, University of Cambridge, Cambridge, United Kingdom.
Wellcome Sanger Institute · GBUniversity of Cambridge · GBWellcome/MRC Cambridge Stem Cell Institute · GBNHS Blood and Transplant · GB

Funding

Cancer Research UK 14953Cancer Research UK C45041/A14953Medical Research Council MC_U105161083Medical Research Council MR/L003368/1Wellcome Trust 084183/Z/07/ZWellcome Trust 97922
6 · The paper itself

Abstract

Ribosome biogenesis is a ubiquitous and essential process in cells. Defects in ribosome biogenesis and function result in a group of human disorders, collectively known as ribosomopathies. In this study, we describe a zebrafish mutant with a loss-of-function mutation in nol9, a gene that encodes a non-ribosomal protein involved in rRNA processing. nol9sa1022/sa1022 mutants have a defect in 28S rRNA processing. The nol9sa1022/sa1022 larvae display hypoplastic pancreas, liver and intestine and have decreased numbers of hematopoietic stem and progenitor cells (HSPCs), as well as definitive erythrocytes and lymphocytes. In addition, ultrastructural analysis revealed signs of pathological processes occurring in endothelial cells of the caudal vein, emphasizing the complexity of the phenotype observed in nol9sa1022/sa1022 larvae. We further show that both the pancreatic and hematopoietic deficiencies in nol9sa1022/sa1022 embryos were due to impaired cell proliferation of respective progenitor cells. Interestingly, genetic loss of Tp53 rescued the HSPCs but not the pancreatic defects. In contrast, activation of mRNA translation via the mTOR pathway by L-Leucine treatment did not revert the erythroid or pancreatic defects. Together, we present the nol9sa1022/sa1022 mutant, a novel zebrafish ribosomopathy model, which recapitulates key human disease characteristics. The use of this genetically tractable model will enhance our understanding of the tissue-specific mechanisms following impaired ribosome biogenesis in the context of an intact vertebrate.

Indexed as

AnimalsDisease Models, AnimalHematopoiesisHematopoietic Stem CellsHumansMorphogenesisPancreasPolynucleotide 5'-Hydroxyl-KinaseRibosomesRNA, Ribosomal, 28STumor Suppressor Protein p53ZebrafishNOL9 protein, humanPolynucleotide 5'-Hydroxyl-KinaseRNA, Ribosomal, 28STP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID26624285
PMCPMC4666468
OpenAlexW2188023805

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.