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.
IN THIS ISSUE| 22 December 2003
FGF8 signalling in development and disease
Online Issn: 1477-9129
Print Issn: 0950-1991
© The Company of Biologists Limited 2003
Development (2003) 130 (25): e2505.
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FGF8 signalling in development and disease. Development 22 December 2003; 130 (25): e2505. doi:
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