PUBLICATION
Stochastic cell-cycle entry and cell-state-dependent fate outputs of injury-reactivated tectal radial glia in zebrafish
- Authors
- Yu, S., He, J.
- ID
- ZDB-PUB-190826-8
- Date
- 2019
- Source
- eLIFE 8: (Journal)
- Registered Authors
- He, Jie, Yu, Shuguang
- Keywords
- Notch, developmental biology, gliosis, injury, radial glia, reactivation, regenerative medicine, stem cells, the optic tectum, zebrafish
- MeSH Terms
-
- Wounds and Injuries/complications*
- Superior Colliculi/injuries*
- Neuroglia/physiology*
- Animals
- Disease Models, Animal
- Cell Proliferation
- Zebrafish
- Cell Cycle*
- Gliosis/physiopathology*
- PubMed
- 31442201 Full text @ Elife
Citation
Yu, S., He, J. (2019) Stochastic cell-cycle entry and cell-state-dependent fate outputs of injury-reactivated tectal radial glia in zebrafish. eLIFE. 8.
Abstract
Gliosis defined as reactive changes of resident glia is the primary response of the central nervous system (CNS) to trauma. The proliferation and fate controls of injury-reactivated glia are essential but remain largely unexplored. In zebrafish optic tectum, we found that stab injury drove a subset of radial glia (RG) into the cell cycle, and surprisingly, proliferative RG responding to sequential injuries of the same site were distinct but overlapping, which was in agreement with stochastic cell-cycle entry. Single-cell RNA sequencing analysis and functional assays further revealed the involvement of Notch/Delta lateral inhibition in this stochastic cell-cycle entry. Furthermore, the long-term clonal analysis showed that proliferative RG were largely gliogenic. Notch inhibition of reactive RG, not dormant and proliferative RG, resulted in an increased production of neurons, which were short-lived. Our findings gain new insights into the proliferation and fate controls of injury-reactivated CNS glia in zebrafish.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping