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First published online November 17, 2003

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FGF8 signalling in development and disease

Mice in which FGF8 expression is globally reduced throughout development have severe cardiovascular and pharyngeal defects at birth, similar to those seen in human 22q11 deletion syndromes such as Di George syndrome. On p. 6361, Macatee et al. suggest that these defects result from a failure in local FGF8 signalling from specific domains of epithelial cells in the pharyngeal arches to the mesenchymal cells that populate and migrate through the arches. To test their hypothesis, the researchers generated Fgf8 conditional alleles and Cre recombinase-expressing drivers designed to ablate FGF8 in different spaciotemporal domains. Ablation of ectodermal FGF8 expression caused defects in aortic arch and coronary vessel formation, whereas ablation of expression in the pharyngeal ectoderm and endoderm caused glandular and valvar defects. These results begin to reveal how local disruptions in FGF8 signalling can produce a spectrum of birth defects.

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Ablation of specific expression domains reveals discrete functions of ectoderm- and endoderm-derived FGF8 during cardiovascular and pharyngeal development

Timothy L. Macatee, Benjamin P. Hammond, Benjamin R. Arenkiel, Lily Francis, Deborah U. Frank, and Anne M. Moon
Development 2003 130: 6361-6374. [Abstract] [Full Text]  

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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Search for Related Content