Evidence map›Paper›PMID 27031842›Full record

ArticleInvestigative ophthalmology & visual science2016

Sox2-Deficient Müller Glia Disrupt the Structural and Functional Maturation of the Mammalian Retina.

Amelia R Bachleda, Larysa H Pevny, Ellen R Weiss

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

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  13. Low availability of cholineFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
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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

3 authors at 2 institutions in 1 country.

Amelia R BachledaNeuroscience Center, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, United States 2Curriculum in Neurobiology, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, United States.
Larysa H PevnyNeuroscience Center, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, United States 3Department of Genetics, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, United States.
Ellen R WeissNeuroscience Center, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, United States 4Department of Cell Biology and Physiology, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, United States 5Lineberger Comprehe.
University of North Carolina at Chapel Hill · USUNC Lineberger Comprehensive Cancer Center

Funding

VISION RESEARCHP30EY005722 · NEI · DUKE UNIVERSITY · PI Vadim Y Arshavsky · 1985 to 2026
$19.3M
DESENSITIZATION OF CONE VISUAL SIGNALING PATHWAYSR01EY012224 · NEI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WEISS, ELLEN RUTH · 2000 to 2019
$5.4M
SOX2 maintains quiescent progenitor cell state of retinal Muller gliaR01EY022341 · NEI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WEISS, ELLEN RUTH · 2012 to 2014
$1.0M
NEI NIH HHS P30 EY005722NEI NIH HHS P30EY05722NEI NIH HHS R01 EY012224NEI NIH HHS R01EY012224NEI NIH HHS R01 EY022341NEI NIH HHS R01EY022341
6 · The paper itself

Abstract

purposeMüller glia (MG), the principal glial cells of the vertebrate retina, display quiescent progenitor cell characteristics. They express key progenitor markers, including the high mobility group box transcription factor SOX2 and maintain a progenitor-like morphology. In the embryonic and mature central nervous system, SOX2 maintains neural stem cell identity. However, its function in committed Müller glia has yet to be determined.

methodsWe use inducible, MG-specific genetic ablation of Sox2 in vivo at the peak of MG genesis to analyze its function in the maturation of murine MG and effects on other cells in the retina. Histologic and functional analysis of the Sox2-deficient retinas is conducted at key points in postnatal development.

resultsAblation of Sox2 in the postnatal retina results in disorganization of MG processes in the inner plexiform layer and mislocalized cell bodies in the nuclear layers. This disorganization is concurrent with a thinning of the neural retina and disruption of neuronal processes in the inner and outer plexiform layers. Functional analysis by electroretinography reveals a decrease in the b-wave amplitude. Disruption of MG maturation due to Sox2 ablation therefore negatively affected the function of the retina.

conclusionsThese results demonstrate a novel role for SOX2 in glial process outgrowth and adhesion, and provide new insights into the essential role Müller glia play in the development of retinal cytoarchitecture. Prior to this work, SOX2 was known to have a primary role in determining cell fate. Our experiments bypass cell fate conversion to establish a new role for SOX2 in a committed cell lineage.

Indexed as

Gene Expression Regulation, DevelopmentalAgingAnimalsCell DifferentiationCell ProliferationElectroretinographyEpendymoglial CellsImmunohistochemistryMiceMice, TransgenicMicroscopy, ElectronNeurogliaRetinaRNASOXB1 Transcription FactorsRNASOXB1 Transcription Factors

Identifiers

PMID27031842
PMCPMC4819558
OpenAlexW2333015395

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.