Evidence map›Paper›PMID 20017954›Full record

ArticleMolecular brain2009

The transcription factor RBP-J is essential for retinal cell differentiation and lamination.

Min-Hua Zheng, Ming Shi, Zhe Pei, Fang Gao, Hua Han, Yu-Qiang Ding

Abstract read
In one paragraph

Article in Molecular brain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Trial
  2. Development of Retinal Astroglia.Annual review of vision science · 2025
    Review
  3. A framework to identify functional interactors that contribute to disrupted early retinal development in Vsx2 ocular retardation J mice.Developmental dynamics : an official publication of the American Association of Anatomists · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Simultaneous Requirements forThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  10. Article
  11. Article
  12. Neurogenesis and Specification of Retinal Ganglion Cells.International journal of molecular sciences · 2020
    Review
  13. Review
  14. Transcription factor Ptf1a in development, diseases and reprogramming.Cellular and molecular life sciences : CMLS · 2019
    Review
  15. Article
  16. Article
  17. Separate and coincident expression of Hes1 and Hes5 in the developing mouse eye.Developmental dynamics : an official publication of the American Association of Anatomists · 2018
    Article
  18. Article
  19. Cell autonomous and nonautonomous requirements for Delltalike1 during early mouse retinal neurogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2016
    Article
  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

6 authors.

Min-Hua ZhengDepartment of Medical Genetics and Developmental Biology, Fourth Military Medical University, Xi'an 710032, China. zhengmh1980@gmail.com
Ming Shi
Zhe Pei
Fang Gao
Hua Han
Yu-Qiang Ding

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe highly ordered vertebrate retina is composed of seven cell types derived from a common pool of retinal progenitor cells (RPCs), and is a good model for the studies of cell differentiation and interaction during neural development. Notch signaling plays a pivotal role in retinogenesis in mammals, but the full scope of the functions of Notch pathway, and the underlying molecular mechanisms, remain unclear.

resultsIn this study, we conditionally knocked out RBP-J, the critical transcription factor downstream to all four Notch receptors, in RPCs of mouse retina at different developmental stages. Disruption of RBP-J at early retinogenesis resulted in accelerated RPCs differentiation, but only photoreceptors and ganglion cells were overrepresented, with other neuronal populations diminished. Similarly, deletion of RBP-J at early postnatal days also led to overproduction of photoreceptors, suggesting that RBP-J governed RPCs specification and differentiation through retinogenesis. In all the RBP-J deletion models, the retinal laminar structures were distorted by the formation of numerous rosette-like structures, reminiscent of beta-catenin deficient retina. Indeed, we found that these rosettes aligned with gaps in beta-catenin expression at the apical surface of the retina. By in vivo electroporation-mediated transfection, we demonstrated that lamination defects in RBP-J deficient retinae were rescued by overexpressing beta-catenin.

conclusionsOur data indicate that RBP-J-mediated canonical Notch signaling governs retinal cell specification and differentiation, and maintains retinal lamination through the expression of beta-catenin.

Indexed as

Cell DifferentiationAnimalsAnimals, NewbornApoptosisbeta CateninCell ProliferationGene DeletionImmunoglobulin J Recombination Signal Sequence-Binding ProteinIntegrasesInterneuronsMiceMice, Inbred C57BLOrganogenesisOrgan SizePhotoreceptor Cells, VertebrateRetinabeta CateninCre recombinaseImmunoglobulin J Recombination Signal Sequence-Binding ProteinIntegrasesRbpj protein, mouseTranscription Factors

Identifiers

PMID20017954
PMCPMC2804697

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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.