Evidence map›Paper›PMID 32562755›Full record

ArticleDevelopmental biology2020

Prdm1 overexpression causes a photoreceptor fate-shift in nascent, but not mature, bipolar cells.

Noah B Goodson, Ko U Park, Jason S Silver, Vince A Chiodo, William W Hauswirth, Joseph A Brzezinski

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Noah B GoodsonDepartment of Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; Neuroscience Graduate Program, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Ko U ParkDepartment of Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Jason S SilverMedical Scientist Training Program, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Vince A ChiodoDepartment of Ophthalmology, University of Florida, Gainesville, FL, USA.
William W HauswirthDepartment of Ophthalmology, University of Florida, Gainesville, FL, USA.
Joseph A BrzezinskiDepartment of Ophthalmology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. Electronic address: Joseph.Brzezinski@cuanschutz.edu.
University of Colorado Anschutz Medical Campus · USUniversity of Florida · US

Funding

Mechanisms of cell fate specification and competence regulation in photoreceptorsR01EY024272 · NEI · UNIVERSITY OF COLORADO DENVER · PI Joseph A Brzezinski · 2014 to 2026
$5.3M
NRSA Training CoreTL1TR002533 · NCATS · UNIVERSITY OF COLORADO DENVER · PI CICUTTO, LISA · 2018 to 2022
$3.0M
Neuroscience Training GrantT32NS099042 · NINDS · UNIVERSITY OF COLORADO DENVER · PI Nidia Calero, GIDON S FELSEN · 2016 to 2026
$2.1M
NCATS NIH HHS TL1 TR002533NEI NIH HHS R01 EY024272NINDS NIH HHS T32 NS099042
6 · The paper itself

Abstract

The transcription factors Prdm1 (Blimp1) and Vsx2 (Chx10) work downstream of Otx2 to regulate photoreceptor and bipolar cell fates in the developing retina. Mice that lack Vsx2 fail to form bipolar cells while Prdm1 mutants form excess bipolars at the direct expense of photoreceptors. Excess bipolars in Prdm1 mutants appear to derive from rods, suggesting that photoreceptor fate remains mutable for some time after cells become specified. Here we tested whether bipolar cell fate is also plastic during development. To do this, we created a system to conditionally misexpress Prdm1 at different stages of bipolar cell development. We found that Prdm1 blocks bipolar cell formation if expressed before the fate choice decision occurred. When we misexpressed Prdm1 just after the decision to become a bipolar cell was made, some cells were reprogrammed into photoreceptors. In contrast, Prdm1 misexpression in mature bipolar cells did not affect cell fate. We also provide evidence that sustained misexpression of Prdm1 was selectively toxic to photoreceptors. Our data show that bipolar fate is malleable, but only for a short temporal window following fate specification. Prdm1 and Vsx2 act by stabilizing photoreceptor and bipolar fates in developing OTX2+ cells of the retina.

Indexed as

Cellular ReprogrammingGene Expression Regulation, DevelopmentalAnimalsHomeodomain ProteinsMiceMice, TransgenicMutationOtx Transcription FactorsPhotoreceptor Cells, VertebratePositive Regulatory Domain I-Binding Factor 1Transcription FactorsHomeodomain ProteinsOtx2 protein, mouseOtx Transcription FactorsPositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouseTranscription FactorsVsx2 protein, mouseBipolar cellsPhotoreceptorsPRDM1Retinal developmentVSX2

Identifiers

PMID32562755
PMCPMC7386070
OpenAlexW3036506974

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.