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Hypogonadotropic hypogonadism and peripheral neuropathy in Ebf2-null mice

MPG-Autoren

Broccoli,  V
Max Planck Institute of Psychiatry, Max Planck Society;

Wurst,  W
Max Planck Institute of Psychiatry, Max Planck Society;

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Zitation

Corradi, A., Croci, L., Broccoli, V., Zecchini, S., Previtali, S., Wurst, W., et al. (2003). Hypogonadotropic hypogonadism and peripheral neuropathy in Ebf2-null mice. Development, 130(2), 401-410.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-000E-9F59-7
Zusammenfassung
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 EbJ2 (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 developmen