PUBLICATION
Wnt/beta-catenin and Fgf signaling control collective cell migration by restricting chemokine receptor expression
- Authors
- Aman, A., and Piotrowski, T.
- ID
- ZDB-PUB-081114-13
- Date
- 2008
- Source
- Developmental Cell 15(5): 749-761 (Journal)
- Registered Authors
- Aman, Andy, Piotrowski, Tatjana
- Keywords
- DEVBIO
- MeSH Terms
-
- Animals
- Cell Movement*
- Fibroblast Growth Factors/metabolism*
- Gene Expression Regulation, Developmental
- Neoplasms/metabolism
- Receptors, CXCR/metabolism*
- Receptors, CXCR4/metabolism*
- Signal Transduction*
- Wnt Proteins/metabolism
- Zebrafish/embryology*
- Zebrafish/metabolism
- Zebrafish Proteins/metabolism*
- beta Catenin/metabolism*
- PubMed
- 19000839 Full text @ Dev. Cell
Citation
Aman, A., and Piotrowski, T. (2008) Wnt/beta-catenin and Fgf signaling control collective cell migration by restricting chemokine receptor expression. Developmental Cell. 15(5):749-761.
Abstract
Collective cell migration is a hallmark of embryonic morphogenesis and cancer metastases. However, the molecular mechanisms regulating coordinated cell migration remain poorly understood. A genetic dissection of this problem is afforded by the migrating lateral line primordium of the zebrafish. We report that interactions between Wnt/beta-catenin and Fgf signaling maintain primordium polarity by differential regulation of gene expression in the leading versus the trailing zone. Wnt/beta-catenin signaling in leader cells informs coordinated migration via differential regulation of the two chemokine receptors, cxcr4b and cxcr7b. These findings uncover a molecular mechanism whereby a migrating tissue maintains stable, polarized gene expression domains despite periodic loss of whole groups of cells. Our findings also bear significance for cancer biology. Although the Fgf, Wnt/beta-catenin, and chemokine signaling pathways are well known to be involved in cancer progression, these studies provide in vivo evidence that these pathways are functionally linked.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping