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Journal of Cell Science, Vol 114, Issue 6 1179-1187, Copyright © 2001 by Company of Biologists
JOURNAL ARTICLES |
HN Dawson, A Ferreira, MV Eyster, N Ghoshal, LI Binder and MP Vitek
Division of Neurology, Department of Medicine, Duke University, Durham, NC 27710 and OSV, Inc., Research Triangle Park, NC 27709, USA. dawso009@mc.duke.edu
Conflicting evidence supports a role for &tgr; 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 &tgr; in axonogenesis, we created &tgr; deficient mice by disrupting the TAU gene. The engineered mice do not express the &tgr; protein, appear physically normal and are able to reproduce. In contrast to a previously reported &tgr; knockout mouse, embryonic hippocampal cultures from &tgr; 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 &tgr; knockout neurons. By mating human TAU-gene transgenic and &tgr; knockout mice, we reconstituted &tgr;-deficient neurons with human &tgr; proteins and restored a normal pattern of axonal growth and neuronal maturation. The ability of human &tgr; proteins to rescue &tgr;-deficient mouse neurons confirms that &tgr; expression affects the rate of neurite extension.
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