Evidence map›Paper›PMID 34415582›Full record

ArticleGlia2021

Notch signaling via Hey1 and Id2b regulates Müller glia's regenerative response to retinal injury.

Aresh Sahu, Sulochana Devi, Jonathan Jui, Daniel Goldman

Open access · greenAbstract read
In one paragraph

Article in Glia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. eLife · 2026
    Article
  5. The long noncoding RNAbioRxiv : the preprint server for biology · 2025
    Article
  6. Article
  7. Article
  8. Timing neural development and regeneration.Current opinion in neurobiology · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Cell-Based Therapies: Strategies for Regeneration.Cold Spring Harbor perspectives in medicine · 2023
    Review
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

4 authors at 1 institution in 1 country.

Aresh SahuMichigan Neuroscience Institute and Department of Biological Chemistry, University of Michigan, Ann Arbor, Michigan, USA.ORCID 0000-0001-8673-9807
Sulochana DeviMichigan Neuroscience Institute and Department of Biological Chemistry, University of Michigan, Ann Arbor, Michigan, USA.
Jonathan JuiMichigan Neuroscience Institute and Department of Biological Chemistry, University of Michigan, Ann Arbor, Michigan, USA.
Daniel GoldmanMichigan Neuroscience Institute and Department of Biological Chemistry, University of Michigan, Ann Arbor, Michigan, USA.ORCID 0000-0002-0013-1188
University of Michigan · US

Funding

Mechanisms underlying Muller glia’s regenerative potentialR01EY032867 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GOLDMAN, DANIEL J · 2021 to 2025
$1.9M
Muller glia heterogeneity and progenitor fateR01EY027310 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GOLDMAN, DANIEL J · 2017 to 2020
$1.2M
NEI NIH HHS R01 EY027310NEI NIH HHS R01 EY032867
6 · The paper itself

Abstract

Zebrafish Müller glia (MG) respond to retinal injury by suppressing Notch signaling and producing progenitors for retinal repair. A certain threshold of injury-derived signal must be exceeded in order to engage MG in a regenerative response (MG's injury-response threshold). Pan-retinal Notch inhibition expands the zone of injury-responsive MG at the site of focal injury, suggesting that Notch signaling regulates MG's injury-response threshold. We found that Notch signaling enhanced chromatin accessibility and gene expression at a subset of regeneration-associated genes in the uninjured retina. Two Notch effector genes, hey1 and id2b, were identified that reflect bifurcation of the Notch signaling pathway, and differentially regulate MG's injury-response threshold and proliferation of MG-derived progenitors. Furthermore, Notch signaling component gene repression in the injured retina suggests a role for Dll4, Dlb, and Notch3 in regulating Notch signaling in MG and epistasis experiments confirm that the Dll4/Dlb-Notch3-Hey1/Id2b signaling pathway regulates MG's injury-response threshold and proliferation.

Indexed as

Basic Helix-Loop-Helix ProteinsNeurogliaReceptors, NotchZebrafishZebrafish ProteinsAnimalsCell ProliferationRetinaSignal TransductionBasic Helix-Loop-Helix Proteinshey1 protein, zebrafishReceptors, NotchZebrafish ProteinsAscl1dll4notch3reprogrammingstem cellzebrafish

Identifiers

PMID34415582
PMCPMC8502208
OpenAlexW3193401683

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.