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
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
Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes