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The Journal of Neuroscience, May 1, 1998, 18(9):3344-3350
Bcl-2 Accelerates the Maturation of Early Sensory Neurons
Gayle
Middleton,
Luzia
G. P. Piñón,
Sean
Wyatt, and
Alun M.
Davies
School of Biological and Medical Sciences, Bute Medical Buildings,
University of St. Andrews, St. Andrews, Fife KY16 9AJ, Scotland.
Bcl-2 is a cytoplasmic protein that blocks apoptosis in a wide
variety of cell types. Here we report a novel role for Bcl-2 in the
early stages of neuronal development. Shortly after differentiating from progenitor cells, sensory neurons undergo a distinct morphological change; initially they have small, spindle-shaped, phase-dark cell
bodies that become large, spherical, and phase-bright. Early sensory
neurons cultured from the trigeminal ganglia of
bcl-2 / embryos at embryonic day
11 (E11) and E12 underwent this change more slowly than trigeminal
neurons of wild-type embryos of the same ages. The delay was not
attributable to the well documented role of Bcl-2 in preventing
apoptosis, because Bcl-2-deficient early sensory neurons survived as
well as wild-type neurons. Accordingly, there was a significantly
smaller number of the more mature type of neuron in the early
trigeminal ganglia of bcl-2/
embryos, yet the number of neurons in the trigeminal ganglia of
bcl-2/ and wild-type embryos was
similar. The absence of Bcl-2 did not cause a uniform delay in the
developmental program of sensory neurons, because the time course of
nerve growth factor receptor expression (both trkA and p75) was
unaffected in the trigeminal neurons of
bcl-2/ embryos. These findings
indicate that Bcl-2 expression is required for the normal progression
of a particular early maturational change in embryonic sensory
neurons.
Key words:
Bcl-2; neuronal differentiation; apoptosis; neurotrophin; sensory neuron; gene-targeted mice
Copyright © 1998 Society for Neuroscience 0270-6474/98/1893344-07$05.00/0
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