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First published online April 12, 2006
doi: 10.1242/10.1242/dev.02324
1 Department of Anatomy, University of California, San Francisco, CA 94143-2711,
USA.
2 Nina Ireland Laboratory of Developmental Neurobiology, Department of
Psychiatry, University of California, San Francisco, San Francisco, CA
94143-2611, USA.
3 Departments of Neuroscience and Molecular Genetics, Albert Einstein College of
Medicine, Bronx, NY 10461, USA.
4 Instituto de Neurociencias de Alicante CSIC and Universidad Miguel
Hernández, Spain.
5 Department of Biological Sciences, Stanford University, Stanford, CA
94305-5020, USA.
Author for correspondence (e-mail:
john.rubenstein{at}ucsf.edu)
Accepted 29 March 2006
Mouse embryos bearing hypomorphic and conditional null Fgf8 mutations have small and abnormally patterned telencephalons. We provide evidence that the hypoplasia results from decreased Foxg1 expression, reduced cell proliferation and increased cell death. In addition, alterations in the expression of Bmp4, Wnt8b, Nkx2.1 and Shh are associated with abnormal development of dorsal and ventral structures. Furthermore, nonlinear effects of Fgf8 gene dose on the expression of a subset of genes, including Bmp4 and Msx1, correlate with a holoprosencephaly phenotype and with the nonlinear expression of transcription factors that regulate neocortical patterning. These data suggest that Fgf8 functions to coordinate multiple patterning centers, and that modifications in the relative strength of FGF signaling can have profound effects on the relative size and nature of telencephalic subdivisions.
Key words: Fgf8, Forebrain, Patterning, Mouse
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