Journal
DEVELOPMENTAL CELL
Volume 15, Issue 5, Pages 749-761Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2008.10.002
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Funding
- National Science Foundation [0519462]
- American Cancer Research [RSG CCG 114528]
- National Institutes of Health [T32HD007491]
- Division Of Integrative Organismal Systems
- Direct For Biological Sciences [0519462] Funding Source: National Science Foundation
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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.
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