Abstract
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.
Original language | English |
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Pages (from-to) | 401-410 |
Number of pages | 10 |
Journal | Development (Cambridge) |
Volume | 130 |
Issue number | 2 |
DOIs | |
State | Published - Jan 2003 |
Externally published | Yes |
Keywords
- COE2
- Dysmyelination
- Gene targeting
- GnRH neurons
- Homologous recombination
- Knockout
- Neural development
- Neuroendocrine
- Neurogenesis
- Neuronal migration
- O/E3
- Olf/Ebf genes
- Peripheral nerve
- Peripheral neuropathy
- Targeted inactivation