This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Attia, M.
Right arrow Articles by Rogner, U. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Attia, M.
Right arrow Articles by Rogner, U. C.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, September 2007, p. 6093-6102, Vol. 27, No. 17
0270-7306/07/$08.00+0     doi:10.1128/MCB.00789-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Nap1l2 Promotes Histone Acetylation Activity during Neuronal Differentiation{triangledown}

Mikaël Attia,1 Christophe Rachez,2 Antoine De Pauw,1,{dagger} Philip Avner,1 and Ute Christine Rogner1*

Unité de Génétique Moléculaire Murine,1 Unité Postulante de Régulation Epigénétique, CNRS URA 2578, Institut Pasteur, 25 rue du Docteur Roux, 75724 Paris Cedex 15, France2

Received 4 May 2007/ Returned for modification 11 June 2007/ Accepted 13 June 2007

The deletion of the neuronal Nap1l2 (nucleosome assembly protein 1-like 2) 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 and H4. Loss of Nap1l2 results in decreased histone acetylation activity, leading to transcriptional changes in differentiating neurons, which include the marked downregulation of the Cdkn1c (cyclin-dependent kinase inhibitor 1c) 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 nucleosome assembly proteins mediate cell-type-specific mechanisms of establishment/modification of a chromatin-permissive state that can affect neurogenesis and neuronal survival.

* Corresponding author. Mailing address: Unité Génétique Moléculaire Murine, CNRS URA 2578, Institut Pasteur, 25 rue du Docteur Roux, 75724 Paris Cedex 15, France. Phone: 33145688602. Fax: 33145688656. E-mail: urogner{at}pasteur.fr

{triangledown} Published ahead of print on 25 June 2007.

{dagger} Present address: Génétique Oncologique, Institut Curie, 26, rue d'Ulm, 75248 Paris Cedex 5, France.

Molecular and Cellular Biology, September 2007, p. 6093-6102, Vol. 27, No. 17
0270-7306/07/$08.00+0     doi:10.1128/MCB.00789-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Kennerson, M., Nicholson, G., Kowalski, B., Krajewski, K., El-Khechen, D., Feely, S., Chu, S., Shy, M., Garbern, J. (2009). X-linked distal hereditary motor neuropathy maps to the DSMAX locus on chromosome Xq13.1-q21. Neurology 72: 246-252 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»