PUBLICATION
Neurogenic phenotype of mind bomb mutants leads to severe patterning defects in the zebrafish hindbrain
- Authors
- Bingham, S., Chaudhari, S., Vanderlaan, G., Itoh, M., Chitnis, A., and Chandrasekhar, A.
- ID
- ZDB-PUB-031103-4
- Date
- 2003
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 228(3): 451-463 (Journal)
- Registered Authors
- Bingham, Stephanie, Chandrasekhar, Anand, Chitnis, Ajay, Itoh, Motoyuki, Vanderlaan, Gary
- Keywords
- zebrafish, hindbrain, motor neuron, induction, rhombomere, green fluorescent protein, neurogenesis, neuroepithelial cell, Notch-Delta signaling, ventral midline
- MeSH Terms
-
- Animals
- Body Patterning/genetics*
- Cell Differentiation/genetics
- In Situ Hybridization
- Motor Neurons/physiology
- Mutagenesis, Site-Directed
- Phenotype
- Rhombencephalon/embryology*
- Ubiquitin-Protein Ligases/genetics*
- Zebrafish/embryology*
- Zebrafish/genetics*
- Zebrafish Proteins/genetics*
- PubMed
- 14579383 Full text @ Dev. Dyn.
Citation
Bingham, S., Chaudhari, S., Vanderlaan, G., Itoh, M., Chitnis, A., and Chandrasekhar, A. (2003) Neurogenic phenotype of mind bomb mutants leads to severe patterning defects in the zebrafish hindbrain. Developmental Dynamics : an official publication of the American Association of Anatomists. 228(3):451-463.
Abstract
Failure of Notch signaling in zebrafish mind bomb (mib) mutants results in a neurogenic phenotype where an overproduction of early differentiating neurons is accompanied by the loss of later-differentiating cell types. We have characterized in detail the hindbrain phenotype of mib mutants. Hindbrain branchiomotor neurons (BMNs) are reduced in number but not missing in mib mutants. In addition, BMN clusters are frequently fused across the midline in mutants. Mosaic analysis indicates that the BMN patterning and fusion defects in the mib hindbrain arise non-cell autonomously. Ventral midline signaling is defective in the mutant hindbrain, in part due to the differentiation of some midline cells into neural cells. Interestingly, while early hindbrain patterning appears normal in mib mutants, subsequent rhombomere-specific gene expression is completely lost. The defects in ventral midline signaling and rhombomere patterning are accompanied by an apparent loss of neuroepithelial cells in the mutant hindbrain. These observations suggest that, by regulating the differentiation of neuroepithelial cells into neurons, Notch signaling preserves a population of non-neuronal cells that are essential for maintaining patterning mechanisms in the developing neural tube.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping