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Mol. Cell. Biol. doi:10.1128/MCB.00789-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Nap1l2 promotes histone acetylation activity during neuronal differentiation

Unité de Génétique Moléculaire Murine, Unité postulante de Régulation épigénétique, CNRS URA 2578, Institut Pasteur, 25 rue du Docteur Roux, 75724 Paris Cedex 15

^* To whom correspondence should be addressed. Email: urogner{at}pasteur.fr.

	Abstract

Deletion of the neuronal Nucleosome assembly protein 1 like 2 (Nap1l2) gene in mice causes neural tube defects. We demonstrate here that this phenotype correlates with deficiencies in differentiation and increased maintenance of the neural stem cell stage. Nap1l2 associates with chromatin and interacts with histones H3, H4. Loss of Nap1l2 results in decreased histone acetylation activity leading to transcriptional changes in differentiating neurons, which include the marked downregulation of the Cyclin dependent kinase inhibitor 1c (Cdkn1c) gene. Cdkn1c expression normally increases during neuronal differentiation and this correlates with the specific recruitment of the Nap1l2 protein and an increase in acetylated histone H3K9/14 at the site of Cdkn1c transcription. These results lead us to suggest that the Nap1l2 protein plays an important role in regulating transcription in developing neurons via the control of histone acetylation. Our data support the idea that neuronal NAPs mediate cell-type specific mechanisms of establishment/modification of a chromatin permissive state that can affect neurogenesis and neuronal survival.