PUBLICATION

Gene regulatory networks controlling vertebrate retinal regeneration

Authors
Hoang, T., Wang, J., Boyd, P., Wang, F., Santiago, C., Jiang, L., Yoo, S., Lahne, M., Todd, L.J., Jia, M., Saez, C., Keuthan, C., Palazzo, I., Squires, N., Campbell, W.A., Rajaii, F., Parayil, T., Trinh, V., Kim, D.W., Wang, G., Campbell, L.J., Ash, J., Fischer, A.J., Hyde, D.R., Qian, J., Blackshaw, S.
ID
ZDB-PUB-201003-6
Date
2020
Source
Science (New York, N.Y.)   370(6519): (Journal)
Registered Authors
Keywords
none
Datasets
GEO:GSE135406
MeSH Terms
  • Animals
  • Cellular Reprogramming/genetics*
  • Chickens
  • Ependymoglial Cells/cytology*
  • Gene Expression Regulation, Developmental
  • Gene Regulatory Networks*
  • Mice
  • Nerve Regeneration/genetics*
  • Neurogenesis/genetics*
  • RNA-Seq
  • Zebrafish
PubMed
33004674 Full text @ Science
Abstract
Injury induces retinal Müller glia of certain cold-blooded vertebrates, but not mammals, to regenerate neurons. To identify gene regulatory networks that reprogram Müller glia into progenitor cells, we profiled changes in gene expression and chromatin accessibility in Müller glia from zebrafish, chick and mice in response to different stimuli. We identified evolutionarily conserved and species-specific gene networks controlling glial quiescence, reactivity and neurogenesis. In zebrafish and chick, transition from the quiescence to reactivity is essential for retinal regeneration, while in mice a dedicated network suppresses neurogenic competence and restores quiescence. Disruption of nuclear factor I (NFI) transcription factors, which maintain and restore quiescence, induces Müller glia to proliferate and generate neurons in adult mice following injury. These findings may aid in designing therapies to restore retinal neurons lost to degenerative diseases.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping