Evidence map›Paper›PMID 33594190›Full record

ArticleScientific reports2021

A Casz1-NuRD complex regulates temporal identity transitions in neural progenitors.

Pierre Mattar, Christine Jolicoeur, Thanh Dang, Sujay Shah, Brian S Clark, Michel Cayouette

Abstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Microfluidic low-input profiling reveals lncRNA roles in disease.bioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Timing neural development and regeneration.Current opinion in neurobiology · 2025
    Review
  8. Article
  9. Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Article
  11. CASZ1 Is Essential for Skin Epidermal Terminal Differentiation.The Journal of investigative dermatology · 2024
    Article
  12. Review
  13. Article
  14. Article
  15. Direct neuronal reprogramming by temporal identity factors.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Mass spectrometry-based retina proteomics.Mass spectrometry reviews · 2023
    Review
  17. Article
  18. Review
  19. Review
  20. 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

6 authors.

Pierre MattarCellular Neurobiology Research Unit, Institut de Recherches Cliniques de Montréal (IRCM), Montreal, QC, H2W 1R7, Canada. pmattar@ohri.ca.
Christine JolicoeurCellular Neurobiology Research Unit, Institut de Recherches Cliniques de Montréal (IRCM), Montreal, QC, H2W 1R7, Canada.
Thanh DangDepartment of Cell and Molecular Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Sujay ShahDepartment of Cell and Molecular Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Brian S ClarkJohn F. Hardesty, MD, Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Michel CayouetteCellular Neurobiology Research Unit, Institut de Recherches Cliniques de Montréal (IRCM), Montreal, QC, H2W 1R7, Canada. michel.cayouette@ircm.qc.ca.

Funding

Identification of the molecular mechanisms mediating intrinsic control of retinal progenitor competenceR00EY027844 · NEI · WASHINGTON UNIVERSITY · PI CLARK, BRIAN S · 2019 to 2021
$739k
CIHR FDN 159936CIHR PJT 166032NEI NIH HHS R00 EY027844
6 · The paper itself

Abstract

Neural progenitor cells undergo identity transitions during development to ensure the generation different types of neurons and glia in the correct sequence and proportions. A number of temporal identity factors that control these transitions in progenitor competence have been identified, but the molecular mechanisms underlying their function remain unclear. Here, we asked how Casz1, the mammalian orthologue of Drosophila castor, regulates competence during retinal development. We show that Casz1 is required to control the transition between neurogenesis and gliogenesis. Using BioID proteomics, we reveal that Casz1 interacts with the nucleosome remodeling and deacetylase (NuRD) complex in retinal cells. Finally, we show that both the NuRD and the polycomb repressor complexes are required for Casz1 to promote the rod fate and suppress gliogenesis. As additional temporal identity factors have been found to interact with the NuRD complex in other contexts, we propose that these factors might act through this common biochemical process to regulate neurogenesis.

Indexed as

NeurogenesisAnimalsDNA-Binding ProteinsEpendymoglial CellsMi-2 Nucleosome Remodeling and Deacetylase ComplexMiceMice, KnockoutNeural Stem CellsPolycomb-Group ProteinsRetinaTranscription FactorsCASZ1 protein, mouseDNA-Binding ProteinsMi-2 Nucleosome Remodeling and Deacetylase ComplexPolycomb-Group ProteinsTranscription Factors

Identifiers

PMID33594190
PMCPMC7886867

What OpenQuestion holds

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Registered trials

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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.