Modest loss of peripheral axons, muscle atrophy and formation of brain inclusions in mice with targeted deletion of gigaxonin exon 1

J Neurochem. 2008 Oct;107(1):253-64. doi: 10.1111/j.1471-4159.2008.05601.x. Epub 2008 Jul 31.

Abstract

Mutations in the gigaxonin gene are responsible for giant axonal neuropathy (GAN), a progressive neurodegenerative disorder associated with abnormal accumulations of Intermediate Filaments (IFs). Gigaxonin is the substrate-specific adaptor for a new Cul3-E3-ubiquitin ligase family that promotes the proteasome dependent degradation of its partners MAP1B, MAP8 and tubulin cofactor B. Here, we report the generation of a mouse model with targeted deletion of Gan exon 1 (Gan(Deltaexon1;Deltaexon1)). Analyses of the Gan(Deltaexon1;Deltaexon1) mice revealed increased levels of various IFs proteins in the nervous system and the presence of IFs inclusion bodies in the brain. Despite deficiency of full length gigaxonin, the Gan(Deltaexon1;Deltaexon1) mice do not develop overt neurological phenotypes and giant axons reminiscent of the human GAN disease. Nonetheless, at 6 months of age the Gan(Deltaexon1;Deltaexon1) mice exhibit a modest hind limb muscle atrophy, a 10% decrease of muscle innervation and a 27% axonal loss in the L5 ventral roots. This new mouse model should provide a useful tool to test potential therapeutic approaches for GAN disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Axons / metabolism
  • Axons / pathology
  • Brain / metabolism*
  • Brain / physiopathology
  • Cells, Cultured
  • Cytoskeletal Proteins / deficiency*
  • Cytoskeletal Proteins / genetics
  • Cytoskeletal Proteins / metabolism
  • Disease Models, Animal
  • Embryonic Stem Cells
  • Exons / genetics
  • Ganglia, Spinal / metabolism
  • Ganglia, Spinal / pathology
  • Ganglia, Spinal / physiopathology
  • Gene Targeting / methods
  • Inclusion Bodies / genetics
  • Inclusion Bodies / metabolism
  • Inclusion Bodies / pathology
  • Intermediate Filament Proteins / metabolism
  • Mice
  • Mice, Knockout
  • Microtubule-Associated Proteins / metabolism
  • Motor Neurons / metabolism
  • Motor Neurons / pathology
  • Muscle, Skeletal / innervation
  • Muscle, Skeletal / physiopathology
  • Muscular Atrophy / genetics
  • Muscular Atrophy / metabolism*
  • Muscular Atrophy / physiopathology
  • Neurodegenerative Diseases / genetics
  • Neurodegenerative Diseases / metabolism*
  • Neurodegenerative Diseases / physiopathology
  • Peripheral Nervous System Diseases / genetics
  • Peripheral Nervous System Diseases / metabolism*
  • Peripheral Nervous System Diseases / physiopathology
  • Phenotype
  • Spinal Nerve Roots / metabolism
  • Spinal Nerve Roots / pathology
  • Spinal Nerve Roots / physiopathology
  • Wallerian Degeneration / genetics
  • Wallerian Degeneration / metabolism*
  • Wallerian Degeneration / physiopathology

Substances

  • Cytoskeletal Proteins
  • Gan protein, mouse
  • Intermediate Filament Proteins
  • Microtubule-Associated Proteins