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Inhibition of neuronal maturation in primary hippocampal neurons from tau deficient mice.

Conflicting evidence supports a role for tau as an essential neuronal cytoskeletal protein or as a redundant protein whose function can be fulfilled by other microtubule-associated proteins. To investigate the function of tau in axonogenesis, we created tau deficient mice by disrupting the TAU gene. The engineered mice do not express the tau protein, appear physically normal and are able to reproduce. In contrast to a previously reported tau knockout mouse, embryonic hippocampal cultures from tau deficient mice show a significant delay in maturation as measured by axonal and neuritic extensions. The classic technique of selectively enhancing axonal growth by growth on laminin substrates failed to restore normal neuronal maturation of tau knockout neurons. By mating human TAU-gene transgenic and tau knockout mice, we reconstituted tau-deficient neurons with human tau proteins and restored a normal pattern of axonal growth and neuronal maturation. The ability of human tau proteins to rescue tau-deficient mouse neurons confirms that tau expression affects the rate of neurite extension.

Pubmed ID: 11228161

Authors

  • Dawson HN
  • Ferreira A
  • Eyster MV
  • Ghoshal N
  • Binder LI
  • Vitek MP

Journal

Journal of cell science

Publication Data

March 6, 2001

Associated Grants

  • Agency: NIA NIH HHS, Id: AG0946
  • Agency: NIA NIH HHS, Id: AG15307
  • Agency: NIA NIH HHS, Id: AG15383
  • Agency: NINDS NIH HHS, Id: NS39080

Mesh Terms

  • Animals
  • Axons
  • Biological Markers
  • Cell Division
  • Cells, Cultured
  • Female
  • Gene Expression
  • Gene Targeting
  • Hippocampus
  • Humans
  • Laminin
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Microtubule-Associated Proteins
  • Neurons
  • tau Proteins