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Journal of Neuroscience, Vol 14, 7319-7330, Copyright © 1994 by Society for Neuroscience
The T alpha 1 alpha-tubulin promoter specifies gene expression as a function of neuronal growth and regeneration in transgenic mice
A Gloster, W Wu, A Speelman, S Weiss, C Causing, C Pozniak, B Reynolds, E Chang, JG Toma and FD Miller
Center for Neuronal Survival, Montreal Neurological Institute, McGill University, Quebec, Canada.
We have previously demonstrated that one member of the alpha-tubulin
multigene family, termed T alpha 1 in rats, is regulated as a function of
neuronal growth and regeneration. To elucidate the molecular mechanisms
responsible for coupling gene expression to morphological differentiation,
we have isolated the T alpha 1 gene, have fused 1.1 kb of the 5' flanking
region to a nuclear lacZ reporter gene, and have generated transgenic mice.
Analysis of these transgenic mice demonstrated that marker gene expression
was specific to the CNS and PNS, with expression in vivo at embryonic day
13.5 being similar to expression of the endogenous gene. Moreover, the
induction of transgene expression was correlated temporally with neuronal
commitment in developing neural crest-derived peripheral neurons and in the
developing retina. Immunocytochemical analysis of mixed primary embryonic
brain cultures confirmed that transgene expression was specific to neurons,
with the majority of neurons, but not astrocytes or oligodendrocytes,
expressing beta-galactosidase. Transgene expression in vivo was maintained
in developing neurons until early in postnatal life, subsequent to which
its expression decreased coincident with neuronal maturation. The transgene
was then reinduced in regenerating facial motoneurons following unilateral
axotomy of the facial nerve. Thus, 1.1 kb of 5' flanking sequence from the
T alpha 1 gene contains the sequence elements responsible for specifying
gene expression to embryonic neurons and for subsequently regulating gene
expression in both developing and mature neurons as a function of
morphological growth.
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