Evidence map›Paper›PMID 20237275›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Dicer is required for the transition from early to late progenitor state in the developing mouse retina.

Sean A Georgi, Thomas A Reh

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

91 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. MicroRNAs in the Mouse Developing Retina.International journal of molecular sciences · 2023
    Review
  10. Review
  11. Article
  12. Review
  13. Retinal Degeneration Caused by Ago2 Disruption.Investigative ophthalmology & visual science · 2021
    Article
  14. Article
  15. Review
  16. MicroRNA Signatures of the Developing Primate Fovea.Frontiers in cell and developmental biology · 2021
    Article
  17. Review
  18. Article
  19. miR-199 family contributes to regulation of sonic hedgehog expression during craniofacial development.Developmental dynamics : an official publication of the American Association of Anatomists · 2020
    Article
  20. Review

31 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Sean A GeorgiNeurobiology and Behavior Program, Department of Biological Structure, School of Medicine, University of Washington, Seattle, Washington 98195, USA.
Thomas A Reh
University of Washington · US

Funding

Stem Cells in the RetinaR01EY013475 · NEI · UNIVERSITY OF WASHINGTON · PI REH, THOMAS A · 2002 to 2010
$3.5M
NEI NIH HHS R01 EY013475
6 · The paper itself

Abstract

MicroRNAs (miRNAs), small 19-25 nucleotide RNAs that influence gene expression through posttranscriptional regulation of mRNA translation and degradation, have recently emerged as important regulators of neural development. Using conditional knock-out of Dicer, an RNase III enzyme required for miRNA maturation, previous studies have demonstrated an essential role for miRNAs in mouse cortical, inner ear, and olfactory development. However, a previous study (Damiani et al., 2008) using a Chx10cre mouse to delete Dicer in retinal progenitors reported no defects in the retina before the second postnatal week, suggesting that miRNAs are not required for mouse retinal development. In an effort to further study the role of miRNAs during retinal development and resolve this apparent conflict, we conditionally knocked out Dicer using a different (alphaPax6cre) line of transgenic mice. In contrast to the previous study, we demonstrate an essential role for miRNAs during mouse retinal development. In the absence of Dicer in the embryonic retina, production of early generated cell types (ganglion and horizontal cells) is increased, and markers of late progenitors are not expressed. This phenotype persists into postnatal retina, in which we find the Dicer-deficient progenitors fail to generate late-born cell types such as rods and Müller glia but continue to generate ganglion cells. We further characterize the dynamic expression of miRNAs during retinal progenitor differentiation and provide a comprehensive profile of miRNAs expressed during retinal development. We conclude that Dicer is necessary for the developmental change in competence of the retinal progenitor cells.

Indexed as

AnimalsAnimals, NewbornCell DifferentiationDEAD-box RNA HelicasesEndoribonucleasesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroRNAsNeurogenesisRetinaRibonuclease IIIStem CellsDEAD-box RNA HelicasesDicer1 protein, mouseEndoribonucleasesMicroRNAsRibonuclease III

Identifiers

PMID20237275
PMCPMC2853880
OpenAlexW2080885130

What OpenQuestion holds

Textmetadata
LicenceTDM
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.