Regenerative Neurogenesis from Neural Progenitor Cells Requires Injury-Induced Expression of Gata3
- Authors
- Kizil, C., Kyritsis, N., Dudczig, S., Kroehne, V., Freudenreich, D., Kaslin, J., and Brand, M.
- ID
- ZDB-PUB-121205-38
- Date
- 2012
- Source
- Developmental Cell 23(6): 1230-1237 (Journal)
- Registered Authors
- Brand, Michael, Dudczig, Stefanie, Freudenreich, Dorian, Kaslin, Jan, Kizil, Caghan, Kroehne, Volker, Kyritsis, Nikos
- Keywords
- none
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- Brain/metabolism
- Brain Injuries/physiopathology
- Cell Movement
- Cell Proliferation
- Fibroblast Growth Factors/genetics
- Fibroblast Growth Factors/metabolism
- GATA3 Transcription Factor/metabolism*
- Inflammation
- Nerve Regeneration
- Neural Stem Cells/metabolism
- Neural Stem Cells/physiology*
- Neurogenesis*
- Neuroglia/physiology
- Neurons/physiology*
- Signal Transduction
- Telencephalon/cytology
- Telencephalon/metabolism
- Telencephalon/physiology*
- Wound Healing
- Zebrafish
- Zebrafish Proteins/metabolism*
- PubMed
- 23168169 Full text @ Dev. Cell
The adult zebrafish brain, unlike mammalian counterparts, can regenerate after injury owing to the neurogenic capacity of stem cells with radial glial character. We hypothesized that injury-induced regenerative programs might be turned on after injury in zebrafish brain and enable regenerative neurogenesis. Here we identify one such gene—the transcription factor gata3—which is expressed only after injury in different zebrafish organs. Gata3 is required for reactive proliferation of radial glia cells, subsequent regenerative neurogenesis, and migration of the newborn neurons. We found that these regeneration-specific roles of Gata3 are dependent on the injury because Gata3 overexpression in the unlesioned adult zebrafish brain is not sufficient to induce neurogenesis. Thus, gata3 acts as a specific injury-induced proregenerative factor that is essential for the regenerative capacity in vertebrates.