PUBLICATION
Fgf3 is crucial for the generation of monoaminergic cerebrospinal fluid contacting cells in zebrafish
- Authors
- Reuter, I., Jäckels, J., Kneitz, S., Kuper, J., Lesch, K.P., Lillesaar, C.
- ID
- ZDB-PUB-190501-4
- Date
- 2019
- Source
- Biology Open 8(6): (Journal)
- Registered Authors
- Lillesaar, Christina
- Keywords
- Central nervous system, Dopamine, Fgf-signalling, Hypothalamus, Serotonin
- MeSH Terms
- none
- PubMed
- 31036752 Full text @ Biol. Open
Citation
Reuter, I., Jäckels, J., Kneitz, S., Kuper, J., Lesch, K.P., Lillesaar, C. (2019) Fgf3 is crucial for the generation of monoaminergic cerebrospinal fluid contacting cells in zebrafish. Biology Open. 8(6):.
Abstract
In most vertebrates, including zebrafish, the hypothalamic serotonergic cerebrospinal fluid-contacting (CSF-c) cells constitute a prominent population. In contrast to the hindbrain serotonergic neurons, little is known about the development and function of these cells. Here, we identify Fibroblast growth factor (Fgf)3 as the main Fgf ligand controlling the ontogeny of serotonergic CSF-c cells. We show that fgf3 positively regulates the number of serotonergic CSF-c cells, as well as a subset of dopaminergic and neuroendocrine cells in the posterior hypothalamus via control of proliferation and cell survival. Further, expression of the ETS-domain transcription factor etv5b is downregulated after fgf3 impairment. Previous findings identified etv5b as critical for the proliferation of serotonergic progenitors in the hypothalamus, and therefore we now suggest that Fgf3 acts via etv5b during early development to ultimately control the number of mature serotonergic CSF-c cells. Moreover, our analysis of the developing hypothalamic transcriptome shows that the expression of fgf3 is upregulated upon fgf3 loss-of-function, suggesting activation of a self-compensatory mechanism. Together, these results highlight Fgf3 in a novel context as part of a signalling pathway of critical importance for hypothalamic development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping