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be A2B5(-). The polyclonal antibody that was used (anti-NF-
M) was well characterized (Bennett et al., 1984; Bennett
and Dilulo, 1985) and was found not to react with other
types of intermediate filaments on Western blots. In
addition, most of the other flat cells that contained glial
filaments as evidenced by reactivity with antibodies
against GFAP did not exhibit reactivity with NF-M. These
results indicate that the NF-M(+) reactivity in these cells
represents the presence of neurofilament reactivity and not
cross-reactivity with, say, GFAP filaments. The fact that
the NF-M(+) flat cells did not show reactivity with the
monoclonal antibody NF1 which is specific for the heavy
weight triplet protein was curious. This may be explained
by the results of others who have demonstrated that the
expression of the 3 triplet proteins in chicks is not
necessarily coordinate (Bennett et al., 1984; Dahl and
Bignami, 1986) and that the last triplet protein to be
expressed in phosphorylated form is often the heavy weight
one (Dahl and Bignami, 1986; Dahl et al., 1986). In any
case, the presence of neurofilament reactivity in cells
that did not acquire a neuronal morphology is unique.
The lack of new DNA synthesis in all cells that were
A2B5(+) was absolute. In purified cultures this negative
correlation indicates several things. The first is that the
recruited A2B5(+) cells at 1 day in culture did not require
new DNA synthesis for the acquisition of cell surface A2B5