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Journal of Neuroscience, Vol 11, 3507-3519, Copyright © 1991 by Society for Neuroscience
Antibody markers identify a common progenitor to sympathetic neurons and chromaffin cells in vivo and reveal the timing of commitment to neuronal differentiation in the sympathoadrenal lineage
DJ Anderson, JF Carnahan, A Michelsohn and PH Patterson
Howard Hughes Medical Institute, California Institute of Technology, Pasadena 91125.
Using specific antibody markers and double-label immunofluorescence
microscopy, we have followed the fate of progenitor cells in the
sympathoadrenal (SA) sublineage of the neural crest in developing rat
embryos. Such progenitors are first recognizable in the primordial
sympathetic ganglia at embryonic day 11.5 (E11.5), when they express
tyrosine hydroxylase. At this stage, the progenitors also coexpress
neuronal markers such as SCG 10 and neurofilament, together with a series
of chromaffin cell markers called SA 1-5 (Carnhan and Patterson, 1991 a).
The observation of such doubly labeled cells is consistent with the
hypothesis that these cells represent a common progenitor to sympathetic
neurons and adrenal chromaffin cells. Subsequent to E 11.5, expression of
the chromaffin markers is extinguished in the sympathetic ganglia but
retained by cells within the adrenal gland. Concomitant with the loss of
the SA 1-5 immunoreactivity in sympathetic ganglia, a later sympathetic
neuron-specific marker, B2, appears. In dissociated cell suspensions, some
B2+ cells that coexpress SA 1 are seen. This implies a switch in the
antigenic phenotype of developing sympathetic neurons, rather than a
replacement of one cell population by another. The SA 1----B2 transition
does not occur for the majority of cells within the adrenal primordium. In
vitro, most B2+ cells fail to differentiate into chromaffin cells in
response to glucocorticoid. Instead, they continue to extend neurites and
then die. Taken together, these data imply that the SA 1----B2 transition
correlates with a loss of competence to respond to an inducer of chromaffin
differentiation. Thus, the development of SA derivatives is controlled both
by environmental signals and by changes in the ability of differentiating
cells to respond to such signals.
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