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Science 302 (5646): 885-889

Copyright © 2003 by the American Association for the Advancement of Science

Derepression of BDNF Transcription Involves Calcium-Dependent Phosphorylation of MeCP2

Wen G. Chen,1,2 Qiang Chang,3 Yingxi Lin,1 Alexander Meissner,3,4 Anne E. West,1 Eric C. Griffith,1 Rudolf Jaenisch,3,4 Michael E. Greenberg1,2*

Abstract: Mutations in MeCP2, which encodes a protein that has been proposed to function as a global transcriptional repressor, are the cause of Rett syndrome (RT T), an X-linked progressive neurological disorder. Although the selective inactivation of MeCP2 in neurons is sufficient to confer a Rett-like phenotype in mice, the specific functions of MeCP2 in postmitotic neurons are not known. We find that MeCP2 binds selectively to BDNF promoter III and functions to repress expression of the BDNF gene. Membrane depolarization triggers the calcium-dependent phosphorylation and release of MeCP2 from BDNF promoter III, thereby facilitating transcription. These studies indicate that MeCP2 plays a key role in the control of neuronal activity–dependent gene regulation and suggest that the deregulation of this process may underlie the pathology of RT T.

1 Division of Neuroscience, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
2 Program in Biological and Biomedical Sciences, Harvard Medical School, Boston, MA 02115, USA.
3 Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
4 Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.

* To whom correspondence should be addressed. E-mail: Michael.Greenberg{at}tch.harvard.edu

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H. M. Abdolmaleky, K.-h. Cheng, S. V. Faraone, M. Wilcox, S. J. Glatt, F. Gao, C. L. Smith, R. Shafa, B. Aeali, J. Carnevale, et al. (2006)
Hum. Mol. Genet. 15, 3132-3145
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Functional Consequences of Mutations in CDKL5, an X-linked Gene Involved in Infantile Spasms and Mental Retardation.
I. Bertani, L. Rusconi, F. Bolognese, G. Forlani, B. Conca, L. De Monte, G. Badaracco, N. Landsberger, and C. Kilstrup-Nielsen (2006)
J. Biol. Chem. 281, 32048-32056
   Abstract »    Full Text »    PDF »
Dysregulation of brain-derived neurotrophic factor expression and neurosecretory function in mecp2 null mice..
H. Wang, S.-a. Chan, M. Ogier, D. Hellard, Q. Wang, C. Smith, and D. M. Katz (2006)
J. Neurosci. 26, 10911-10915
   Abstract »    Full Text »    PDF »
MBD2 is a critical component of a methyl cytosine-binding protein complex isolated from primary erythroid cells.
E. P. Kransdorf, S. Z. Wang, S. Z. Zhu, T. B. Langston, J. W. Rupon, and G. D. Ginder (2006)
Blood 108, 2836-2845
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Control of the DNA Methylation System Component MBD2 by Protein Arginine Methylation.
C. P. Tan and S. Nakielny (2006)
Mol. Cell. Biol. 26, 7224-7235
   Abstract »    Full Text »    PDF »
Neurotrophin-regulated signalling pathways.
L. F Reichardt (2006)
Phil Trans R Soc B 361, 1545-1564
   Abstract »    Full Text »    PDF »
MBD family proteins: reading the epigenetic code.
M. Fatemi and P. A. Wade (2006)
J. Cell Sci. 119, 3033-3037
   Abstract »    Full Text »    PDF »
Fluoxetine and Cocaine Induce the Epigenetic Factors MeCP2 and MBD1 in Adult Rat Brain.
S. Cassel, D. Carouge, C. Gensburger, P. Anglard, C. Burgun, J.-B. Dietrich, D. Aunis, and J. Zwiller (2006)
Mol. Pharmacol. 70, 487-492
   Abstract »    Full Text »    PDF »
Chromatin Remodeling: A Novel Mechanism of Psychotropic Drug Action.
S. S. Newton and R. S. Duman (2006)
Mol. Pharmacol. 70, 440-443
   Abstract »    Full Text »    PDF »

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