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RESEARCH PAPER
1 Sensory Development, Riken Center for Developmental Biology, Chuo-ku, Kobe 650-0047, Japan; 2 Department of Neurobiology and Anatomy and 3 Children's Health Research Center, University of Utah School of Medicine, Salt Lake City, Utah 84132-3401, USA; 4 Department of Human Genetics and 5 Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah 84112-5330, USA
In both chick and mouse, the otic placode, the rudiment of the inner ear, is induced by at least two signals, one from the cephalic paraxial mesoderm and the other from the neural ectoderm. In chick, the mesodermal signal, FGF19, induces neural ectoderm to express additional signals, including WNT8c and FGF3, resulting in induction of the otic placode. In mouse, mesodermal Fgf10 acting redundantly with neural Fgf3 is required for induction of the placode. To determine how the mesodermal inducers of the otic placode are localized, we took advantage of the unique strengths of the two model organisms. We show that endoderm is necessary for otic induction in the chick and that Fgf8, expressed in the chick endoderm subjacent to Fgf19, is both sufficient and necessary for the expression of Fgf19 in the mesoderm. In the mouse, Fgf8 is also expressed in endoderm as well as in other germ layers in the periotic placode region. We show that otic induction fails in embryos null for Fgf3 and hypomorphic for Fgf8 and expression of mesodermal Fgf10 is reduced. Thus, Fgf8 plays a critical upstream role in an FGF signaling cascade required for otic induction in chick and mouse.
[Keywords: FGF8; FGF3; FGF10; FGF19; otic; endoderm]
Received October 19, 2004; revised version accepted January 14, 2005.
6 These authors contributed equally to the study.
7 Corresponding author.
E-MAIL raj-ladher{at}cdb.riken.go.jp; FAX 81-78-306-3322
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