PUBLICATION
Fascin1-Dependent Filopodia are Required for Directional Migration of a Subset of Neural Crest Cells
- Authors
- Boer, E.F., Howell, E.D., Schilling, T.F., Jette, C.A., Stewart, R.A.
- ID
- ZDB-PUB-150122-3
- Date
- 2015
- Source
- PLoS Genetics 11: e1004946 (Journal)
- Registered Authors
- Jette, Cicely A., Schilling, Tom, Stewart, Rodney A.
- Keywords
- Embryos, Cell migration, Neuron migration, Zebrafish, Neurons, Ganglia, Cartilage, Cancer cell migration
- MeSH Terms
-
- Animals
- Body Patterning/genetics
- Cell Movement/genetics
- Epithelial-Mesenchymal Transition/genetics
- Gene Expression Regulation, Developmental
- Microfilament Proteins/genetics*
- Mutation
- Neural Crest/cytology
- Neural Crest/growth & development*
- Pseudopodia/genetics*
- Signal Transduction
- Zebrafish/genetics
- Zebrafish/growth & development*
- Zebrafish Proteins/biosynthesis
- Zebrafish Proteins/genetics*
- PubMed
- 25607881 Full text @ PLoS Genet.
Citation
Boer, E.F., Howell, E.D., Schilling, T.F., Jette, C.A., Stewart, R.A. (2015) Fascin1-Dependent Filopodia are Required for Directional Migration of a Subset of Neural Crest Cells. PLoS Genetics. 11:e1004946.
Abstract
Directional migration of neural crest (NC) cells is essential for patterning the vertebrate embryo, including the craniofacial skeleton. Extensive filopodial protrusions in NC cells are thought to sense chemo-attractive/repulsive signals that provide directionality. To test this hypothesis, we generated null mutations in zebrafish fascin1a (fscn1a), which encodes an actin-bundling protein required for filopodia formation. Homozygous fscn1a zygotic null mutants have normal NC filopodia due to unexpected stability of maternal Fscn1a protein throughout NC development and into juvenile stages. In contrast, maternal/zygotic fscn1a null mutant embryos (fscn1a MZ) have severe loss of NC filopodia. However, only a subset of NC streams display migration defects, associated with selective loss of craniofacial elements and peripheral neurons. We also show that fscn1a-dependent NC migration functions through cxcr4a/cxcl12b chemokine signaling to ensure the fidelity of directional cell migration. These data show that fscn1a-dependent filopodia are required in a subset of NC cells to promote cell migration and NC derivative formation, and that perdurance of long-lived maternal proteins can mask essential zygotic gene functions during NC development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping