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Derepression of BDNF Transcription Involves Calcium-Dependent Phosphorylation of MeCP2
Wen G. Chen,1,2Qiang Chang,3Yingxi Lin,1Alexander Meissner,3,4Anne E. West,1Eric C. Griffith,1Rudolf Jaenisch,3,4Michael E. Greenberg1,2*
Mutations in MeCP2, which encodes a protein that has been proposedto function as a global transcriptional repressor, are the causeof Rett syndrome (RT T), an X-linked progressive neurologicaldisorder. Although the selective inactivation of MeCP2 in neuronsis sufficient to confer a Rett-like phenotype in mice, the specificfunctions of MeCP2 in postmitotic neurons are not known. Wefind that MeCP2 binds selectively to BDNF promoter III and functionsto repress expression of the BDNF gene. Membrane depolarizationtriggers the calcium-dependent phosphorylation and release ofMeCP2 from BDNF promoter III, thereby facilitating transcription.These studies indicate that MeCP2 plays a key role in the controlof neuronal activity–dependent gene regulation and suggestthat the deregulation of this process may underlie the pathologyof 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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