RT Journal Article SR Electronic T1 Hypogonadotropic hypogonadism and peripheral neuropathy in Ebf2-null mice JF Development JO Development FD The Company of Biologists Limited SP 401 OP 410 DO 10.1242/dev.00215 VO 130 IS 2 A1 Corradi, Anna A1 Croci, Laura A1 Broccoli, Vania A1 Zecchini, Silvia A1 Previtali, Stefano A1 Wurst, Wolfgang A1 Amadio, Stefano A1 Maggi, Roberto A1 Quattrini, Angelo A1 Consalez, G. Giacomo YR 2003 UL http://dev.biologists.org/content/130/2/401.abstract AB 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.