Evidence map›Paper›PMID 21087508›Full record

ArticleMolecular brain2010

MATH5 controls the acquisition of multiple retinal cell fates.

Liang Feng, Zheng-hua Xie, Qian Ding, Xiaoling Xie, Richard T Libby, Lin Gan

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2010. 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
2.6field-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

56 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
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  3. Lineage tracing revealsbioRxiv : the preprint server for biology · 2026
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  9. Neurog2 regulates Isl1 to modulate horizontal cell number.Development (Cambridge, England) · 2023
    Article
  10. Review
  11. Article
  12. Genetic control of retinal ganglion cell genesis.Cellular and molecular life sciences : CMLS · 2021
    Review
  13. Article
  14. Article
  15. Two new genetically modified mouse alleles labeling distinct phases of retinal ganglion cell development by fluorescent proteins.Developmental dynamics : an official publication of the American Association of Anatomists · 2020
    Article
  16. TheProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Article
  18. Neurogenesis and Specification of Retinal Ganglion Cells.International journal of molecular sciences · 2020
    Review
  19. 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 at 1 institution in 1 country.

Liang FengFlaum Eye Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Zheng-hua Xie
Qian Ding
Xiaoling Xie
Richard T Libby
Lin Gan
University of Rochester · US

Funding

Math5 Regulatory Pathway in Retinal DevelopmentR01EY013426 · NEI · UNIVERSITY OF ROCHESTER · PI GAN, LIN · 2001 to 2010
$2.9M
NEI NIH HHS EY013426NEI NIH HHS R01 EY013426
6 · The paper itself

Abstract

Math5-null mutation results in the loss of retinal ganglion cells (RGCs) and in a concurrent increase of amacrine and cone cells. However, it remains unclear whether there is a cell fate switch of Math5-lineage cells in the absence of Math5 and whether MATH5 cell-autonomously regulates the differentiation of the above retinal neurons. Here, we performed a lineage analysis of Math5-expressing cells in developing mouse retinas using a conditional GFP reporter (Z/EG) activated by a Math5-Cre knock-in allele. We show that during normal retinogenesis, Math5-lineage cells mostly develop into RGCs, horizontal cells, cone photoreceptors, rod photoreceptors, and amacrine cells. Interestingly, amacrine cells of Math5-lineage cells are predominately of GABAergic, cholinergic, and A2 subtypes, indicating that Math5 plays a role in amacrine subtype specification. In the absence of Math5, more Math5-lineage cells undergo cell fate conversion from RGCs to the above retinal cell subtypes, and occasionally to cone-bipolar cells and Müller cells. This change in cell fate choices is accompanied by an up-regulation of NEUROD1, RXRγ and BHLHB5, the transcription factors essential for the differentiation of retinal cells other than RGCs. Additionally, loss of Math5 causes the failure of early progenitors to exit cell cycle and leads to a significant increase of Math5-lineage cells remaining in cell cycle. Collectively, these data suggest that Math5 regulates the generation of multiple retinal cell types via different mechanisms during retinogenesis.

Indexed as

Cell LineageAnimalsApoptosisBasic Helix-Loop-Helix ProteinsBiomarkersCell DifferentiationCell ProliferationEmbryo, MammalianGene Expression Regulation, DevelopmentalMiceMice, KnockoutNerve Tissue ProteinsRetinaRetinal NeuronsAtoh7 protein, mouseBasic Helix-Loop-Helix ProteinsBiomarkersNerve Tissue Proteins

Identifiers

PMID21087508
PMCPMC2994854
OpenAlexW1989972710

What OpenQuestion holds

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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.