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doi: 10.1242/10.1242/dev.00215
DEVELOPMENT AND DISEASE |
1 San Raffaele Scientific Institute, Milan, Italy
2 Stem Cell Research Institute, San Raffaele Scientific Institute, Milan,
Italy
3 Max Planck Institute of Psychiatry, Munich, and GSF-Research Center of
Environment and Health, Institute of Developmental Genetics, Neuherberg,
Germany
4 CEND, Department of Endocrinology, University of Milan, Italy
Author for correspondence (e-mail:
g.consalez{at}hsr.it)
Accepted 18 October 2002
Olf/Ebf transcription factors have been implicated in numerous developmental processes, ranging from B-cell development to neuronal differentiation. We describe mice that carry a targeted deletion within the Ebf2 (O/E3) gene. In Ebf2-null mutants, because of defective migration of gonadotropin releasing hormone-synthesizing neurons, formation of the neuroendocrine axis (which is essential for pubertal development) is impaired, leading to secondary hypogonadism. In addition, Ebf2-/- peripheral nerves feature defective axon sorting, hypomyelination, segmental dysmyelination and axonal damage, accompanied by a sharp decrease in motor nerve conduction velocity. Ebf2-null mice reveal a novel genetic cause of hypogonadotropic hypogonadism and peripheral neuropathy in the mouse, disclosing an important role for Ebf2 in neuronal migration and nerve development.
Key words: Olf/Ebf genes, Neurogenesis, Neural development, Neuronal migration, Neuroendocrine, GnRH neurons, Peripheral nerve, Peripheral neuropathy, Dysmyelination, Homologous recombination, Knockout, Targeted inactivation, Gene targeting, COE2, O/E3
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