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Department of Neurobiology, The Scripps Research Institute and The Skaggs Institute for Chemical Biology, La Jolla,
California 92037
The cell adhesion molecule L1 mediates neurite outgrowth and fasciculation during embryogenesis
and mutations in its gene have been linked to a number
of human congenital syndromes. To identify DNA sequences that restrict expression of L1 to the nervous system, we isolated a previously unidentified segment
of the mouse L1 gene containing the promoter, the first
exon, and the first intron and examined its activity in
vitro and in vivo. We found that a neural restrictive silencer element (NRSE) within the second intron prevented expression of L1 gene constructs in nonneural cells. For optimal silencing of L1 gene expression by the
NRSE-binding factor RE-1-silencing transcription factor (REST)/NRSF, both the NRSE and sequences in
the first intron were required. In transgenic mice, an
L1lacZ gene construct with the NRSE generated a neurally restricted expression pattern consistent with the
known pattern of L1 expression in postmitotic neurons
and peripheral glia. In contrast, a similar construct lacking the NRSE produced precocious expression in the
peripheral nervous system and ectopic expression in
mesenchymal derivatives of the neural crest and in mesodermal and ectodermal cells. These experiments
show that the NRSE and REST/NRSF are important
components in restricting L1 expression to the embryonic nervous system.
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