Hypogonadotropic hypogonadism and peripheral neuropathy in Ebf2-null mice

Anna Corradi, Laura Croci, Vania Broccoli, Silvia Zecchini, Stefano Previtali, Wolfgang Wurst, Stefano Amadio, Roberto Maggi, Angelo Quattrini, G. Giacomo Consalez

Research output: Contribution to journalArticlepeer-review

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 languageEnglish
Pages (from-to)401-410
Number of pages10
JournalDevelopment
Volume130
Issue number2
DOIs
Publication statusPublished - Jan 2003

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

ASJC Scopus subject areas

  • Anatomy
  • Cell Biology

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