PUBLICATION
cxcl18b-defined transitional state-specific nitric oxide drives injury-induced Müller glia cell-cycle re-entry in the zebrafish retina
- Authors
- Ye, A., Yu, S., Du, M., Zhou, D., He, J., Chen, C.
- ID
- ZDB-PUB-260122-1
- Date
- 2026
- Source
- eLIFE 14: (Journal)
- Registered Authors
- He, Jie
- Keywords
- Müller glia, cell-cycle re-entry, cxcl18b, neuroscience, nitric oxide, precision redox, zebrafish, zebrafish retina
- MeSH Terms
-
- Animals
- Cell Cycle*
- Cell Proliferation
- Chemokines, CXC*/genetics
- Chemokines, CXC*/metabolism
- Ependymoglial Cells*/metabolism
- Ependymoglial Cells*/physiology
- Nitric Oxide*/metabolism
- Retina*/injuries
- Retina*/metabolism
- Zebrafish*
- Zebrafish Proteins*/genetics
- Zebrafish Proteins*/metabolism
- PubMed
- 41562588 Full text @ Elife
Citation
Ye, A., Yu, S., Du, M., Zhou, D., He, J., Chen, C. (2026) cxcl18b-defined transitional state-specific nitric oxide drives injury-induced Müller glia cell-cycle re-entry in the zebrafish retina. eLIFE. 14:.
Abstract
In lower vertebrates, retinal Müller glia (MG) exhibit a life-long capacity of cell-cycle re-entry to regenerate neurons following the retinal injury. However, the mechanism driving such injury-induced MG cell-cycle re-entry remains incompletely understood. Combining single-cell transcriptomic analysis and in vivo clonal analysis, we identified previously undescribed cxcl18b-defined MG transitional states as essential routes toward MG proliferation following green/red cone (G/R cone) ablation. Inflammation blockage abolished the triggering of these transitional states, which expressed the gene modules shared by cells of the ciliary marginal zone (CMZ), where life-long adult neurogenesis takes place. Functional studies of the redox properties of these transitional states further demonstrated the regulatory role of nitric oxide (NO) produced by Nos2b in injury-induced MG proliferation. Finally, we developed a viral-based strategy to specifically disrupt nos2b in cxcl18b-defined MG transitional states and revealed the effect of transitional state-specific NO signaling. Our findings elucidate the precision redox mechanism underlying injury-induced MG cell-cycle re-entry, providing insights into species-specific mechanisms for vertebrate retina regeneration.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping