Evidence map›Paper›PMID 24116103›Full record

ArticlePloS one2013

Genetic interactions between Brn3 transcription factors in retinal ganglion cell type specification.

Melody Shi, Sumit R Kumar, Oluwaseyi Motajo, Friedrich Kretschmer, Xiuqian Mu, Tudor C Badea

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–field-weighted citation impact, top 97% 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

32 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Genetic control of retinal ganglion cell genesis.Cellular and molecular life sciences : CMLS · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Wiring the Binocular Visual Pathways.International journal of molecular sciences · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Integral bHLH factor regulation of cell cycle exit and RGC differentiation.Developmental dynamics : an official publication of the American Association of Anatomists · 2018
    Article
  18. Article
  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 2 institutions in 1 country.

Melody ShiNational Eye Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Sumit R Kumar
Oluwaseyi Motajo
Friedrich Kretschmer
Xiuqian Mu
Tudor C Badea
National Institutes of Health · USRoswell Park Comprehensive Cancer Center · US

Funding

Retinal Circuit Development & GeneticsZIAEY000504 · NEI · NATIONAL EYE INSTITUTE · PI BADEA, TUDOR · 2011 to 2021
$15.6M
Regulatory mechanisms for retinal ganglion cell genesisR01EY020545 · NEI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI Xiuqian Mu · 2011 to 2026
$5.7M
Intramural NIH HHSNEI NIH HHS EY020545NEI NIH HHS R01 EY020545
6 · The paper itself

Abstract

backgroundVisual information is conveyed from the retina to the brain via 15-20 Retinal Ganglion Cell (RGC) types. The developmental mechanisms by which RGC types acquire their distinct molecular, morphological, physiological and circuit properties are essentially unknown, but may involve combinatorial transcriptional regulation. Brn3 transcription factors are expressed in RGCs from early developmental stages, and are restricted in adults to distinct, partially overlapping populations of RGC types. Previously, we described cell autonomous effects of Brn3b (Pou4f2) and Brn3a (Pou4f1) on RGC axon and dendrites development. METHODS AND

findingsWe now have investigated genetic interactions between Brn3 transcription factors with respect to RGC development, by crossing conventional knock-out alleles of each Brn3 gene with conditional knock-in reporter alleles of a second Brn3 gene, and analyzing the effects of single or double Brn3 knockouts on RGC survival and morphology. We find that Brn3b loss results in axon defects and dendritic arbor area and lamination defects in Brn3a positive RGCs, and selectively affects survival and morphology of specific Brn3c (Pou4f3) positive RGC types. Brn3a and Brn3b interact synergistically to control RGC numbers. Melanopsin positive ipRGCs are resistant to combined Brn3 loss but are under the transcriptional control of Isl1, expanding the combinatorial code of RGC specification.

conclusionsTaken together these results complete our knowledge on the mechanisms of transcriptional control of RGC type specification. They demonstrate that Brn3b is required for the correct development of more RGC cell types than suggested by its expression pattern in the adult, but that several cell types, including some Brn3a, Brn3c or Melanopsin positive RGCs are Brn3b independent.

Indexed as

Epistasis, GeneticAnimalsCell CountCell SurvivalFemaleGene Expression Regulation, DevelopmentalHomeodomain ProteinsMaleMelanopsinMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMicroscopy, FluorescenceNeurofilament ProteinsRetinaHomeodomain ProteinsMelanopsinneurofilament protein LNeurofilament ProteinsPou4f1 protein, mousePou4f2 protein, mouseRod OpsinsTranscription Factor Brn-3ATranscription Factor Brn-3BTranscription Factor Brn-3C

Identifiers

PMID24116103
PMCPMC3792956
OpenAlexW885746559

What OpenQuestion holds

Textmetadata
LicenceCC0
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.