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The mouse c-src gene contains a short
neuron-specific exon, N1. N1 exon splicing is partly controlled
by an intronic splicing enhancer sequence that activates
splicing of a heterologous reporter exon in both neural
and nonneural cells. Here we attempt to dissect all of
the regulatory elements controlling the N1 exon and examine
how these multiple elements work in combination. We show
that the 3′ splice site sequence upstream of exon
N1 represses the activation of splicing by the downstream
intronic enhancer. This repression is stronger in nonneural
cells and these two regulatory sequences combine to make
a reporter exon highly cell-type specific. Substitution
of the 3′ splice site of this test exon with sites
from other exons indicates that activation by the enhancer
is very dependent on the nature of the upstream 3′
splice site. In addition, we identify a previously uncharacterized
purine-rich sequence within exon N1 that cooperates with
the downstream intronic enhancer to increase exon inclusion.
Finally, different regulatory elements were tested in multiple
cell lines of both neuronal and nonneuronal origin. The
individual splicing regulatory sequences from the src
gene vary widely in their activity between different cell
lines. These results demonstrate how a simple cassette
exon is controlled by a variety of regulatory elements
that only in combination will produce the correct tissue
specificity of splicing.
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