RRC ID 370
Author Bingham S, Chaudhari S, Vanderlaan G, Itoh M, Chitnis A, Chandrasekhar A.
Title Neurogenic phenotype of mind bomb mutants leads to severe patterning defects in the zebrafish hindbrain.
Journal Dev. Dyn.
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.
Volume 228(3)
Pages 451-63
Published 2003-11
DOI 10.1002/dvdy.10429
PMID 14579383
PMC PMC2219915
MeSH 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*
IF 2.852
Times Cited 28
Zebrafish rw0