PUBLICATION
Nodal signalling imposes left-right asymmetry upon neurogenesis in the habenular nuclei
- Authors
- Roussigné, M., Bianco, I.H., Wilson, S.W., and Blader, P.
- ID
- ZDB-PUB-090417-1
- Date
- 2009
- Source
- Development (Cambridge, England) 136(9): 1549-1557 (Journal)
- Registered Authors
- Bianco, Isaac, Blader, Patrick, Roussigné, Myriam, Wilson, Steve
- Keywords
- Nodal signalling, Asymmetry, Habenular nuclei, Neurogenesis, Zebrafish
- MeSH Terms
-
- Animals
- Body Patterning*
- Gene Expression Regulation, Developmental
- Habenula/embryology*
- Habenula/metabolism*
- Neurogenesis*
- Nodal Protein/genetics
- Nodal Protein/metabolism*
- Receptors, CXCR4/genetics
- Receptors, CXCR4/metabolism
- Signal Transduction
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish/metabolism*
- PubMed
- 19363156 Full text @ Development
Citation
Roussigné, M., Bianco, I.H., Wilson, S.W., and Blader, P. (2009) Nodal signalling imposes left-right asymmetry upon neurogenesis in the habenular nuclei. Development (Cambridge, England). 136(9):1549-1557.
Abstract
The habenulae are evolutionarily conserved bilateral nuclei in the epithalamus that relay input from the forebrain to the ventral midbrain. In zebrafish, the habenulae display left-right (L/R) asymmetries in gene expression and axonal projections. The elaboration of habenular asymmetries requires the presence of a second asymmetric structure, the parapineal, the laterality of which is biased by unilateral Nodal signalling. Here we show that neurons are present earlier in the left habenula than in the right, but, in contrast to other habenular asymmetry phenotypes, this asymmetry in neurogenesis is not dependent on the parapineal. Embryos in which the L/R asymmetry in Nodal signalling is abolished display symmetric neurogenesis, revealing a requirement for this pathway in asymmetrically biasing neurogenesis. Our results provide evidence of a direct requirement for unilateral Nodal activity in establishing an asymmetry per se, rather than solely in biasing its laterality.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping