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Nuclear factor I-A represses expression of the cell adhesion molecule L1

Tanja Schneegans1, Uwe Borgmeyer1, Moritz Hentschke12, Richard M Gronostajski34, Melitta Schachner1567 and Thomas Tilling1*

Author affiliations

1 Zentrum für Molekulare Neurobiologie, Universitätsklinikum Hamburg-Eppendorf, D-20246 Hamburg, Germany

2 Institut für Med. Mikrobiologie, Virologie und Hygiene, Universitätsklinikum Hamburg-Eppendorf, D-20246 Hamburg, Germany

3 Department of Biochemistry, State University of New York at Buffalo, Buffalo, NY 14214, USA

4 Developmental Genomics Group, New York State Center of Excellence in Bioinformatics and Life Sciences, Buffalo, NY 14203, USA

5 Keck Center for Collaborative Neuroscience, Rutgers University, Piscataway, NJ 08854, USA

6 Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854, USA

7 Center for Neuroscience, Shantou Medical College, 22 Xin Ling Road, Shantou 515041, PR China

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Citation and License

BMC Molecular Biology 2009, 10:107  doi:10.1186/1471-2199-10-107

Published: 14 December 2009



The neural cell adhesion molecule L1 plays a crucial role in development and plasticity of the nervous system. Neural cells thus require precise control of L1 expression.


We identified a full binding site for nuclear factor I (NFI) transcription factors in the regulatory region of the mouse L1 gene. Electrophoretic mobility shift assay (EMSA) showed binding of nuclear factor I-A (NFI-A) to this site. Moreover, for a brain-specific isoform of NFI-A (NFI-A bs), we confirmed the interaction in vivo using chromatin immunoprecipitation (ChIP). Reporter gene assays showed that in neuroblastoma cells, overexpression of NFI-A bs repressed L1 expression threefold.


Our findings suggest that NFI-A, in particular its brain-specific isoform, represses L1 gene expression, and might act as a second silencer of L1 in addition to the neural restrictive silencer factor (NRSF).