Identification of wnt-responsive cells in the zebrafish hypothalamus
- Wang, X., Lee, J.E., and Dorsky, R.I.
- Zebrafish 6(1): 49-58 (Journal)
- Registered Authors
- Dorsky, Richard, Lee, Ji Eun, Wang, Xu
- MeSH Terms
- Embryo, Nonmammalian
- Hypothalamus/growth & development
- Signal Transduction*
- Stem Cells/metabolism
- TCF Transcription Factors/metabolism
- Transcription Factor 7-Like 1 Protein
- Transcription Factors/metabolism
- Wnt Proteins/metabolism*
- Zebrafish/growth & development*
- Zebrafish Proteins/metabolism
- 19374548 Full text @ Zebrafish
Wang, X., Lee, J.E., and Dorsky, R.I. (2009) Identification of wnt-responsive cells in the zebrafish hypothalamus. Zebrafish. 6(1):49-58.
In all vertebrate brains, there is a period of widespread embryonic neurogenesis followed by specific regional neurogenesis that continues into adult stages. The Wnt signaling pathway, which is essential for numerous developmental processes, has also been suggested to be involved in neurogenesis. To help investigate the exact roles of canonical Wnt signaling in neurogenesis, here we examine the identity of Wnt-responsive cells in the zebrafish hypothalamus. This tissue is a useful diencephalic neurogenesis model containing evolutionarily conserved populations of neurons. We first performed in situ hybridization to show the expression patterns of Tcf family members and a canonical Wnt signaling reporter in the 50 hpf embryonic hypothalamus and larval/adult hypothalamus. We then used immunohistochemistry to identify the cell types of Wnt-responsive and Lef1-positive cells in both 50 hpf embryonic and adult hypothalamus. Our results indicate that Wnt-responsive cells in the hypothalamus are likely to be both mitotic progenitors and postmitotic precursors at embryonic stages, but only precursors at the adult stage. These data suggest that canonical Wnt signaling may be functionally required for maintenance of neural progenitor and precursor pools in the embryo, and for ongoing neurogenesis in the adult zebrafish.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes