de.mpg.escidoc.pubman.appbase.FacesBean
English
 
Help Guide Disclaimer Contact us Login
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Hypogonadotropic hypogonadism and peripheral neuropathy in Ebf2-null mice

MPS-Authors

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

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

Locator
There are no locators available
Fulltext (public)
There are no public fulltexts available
Supplementary Material (public)
There is no public supplementary material available
Citation

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.


Cite as: http://hdl.handle.net/11858/00-001M-0000-000E-9F59-7
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 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