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Nucleic Acids Research Advance Access originally published online on August 13, 2007
Nucleic Acids Research 2007 35(16):5402-5408; doi:10.1093/nar/gkm599
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Nucleic Acids Research, 2007, Vol. 35, No. 16 5402-5408
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


Molecular Biology

MeCP2 interacts with HP1 and modulates its heterochromatin association during myogenic differentiation

Noopur Agarwal1, Tanja Hardt1, Alessandro Brero1, Danny Nowak1, Ulrich Rothbauer2, Annette Becker1, Heinrich Leonhardt2 and M. Cristina Cardoso1,*

1Max Delbrück Center for Molecular Medicine, 13125 Berlin and 2Ludwig Maximilians University Munich, Biocenter, Department of Biology, 82152 Planegg-Martinsried, Germany

*To whom Correspondence should be addressed: Tel: +49 30 94062109; Fax: +49 30 94063343; Email: cardoso{at}mdc-berlin.de

Received March 7, 2007. Revised July 20, 2007. Accepted July 20, 2007.

There is increasing evidence of crosstalk between epigenetic modifications such as histone and DNA methylation, recognized by HP1 and methyl CpG-binding proteins, respectively. We have previously shown that the level of methyl CpG-binding proteins increased dramatically during myogenesis leading to large-scale heterochromatin reorganization. In this work, we show that the level of HP1 isoforms did not change significantly throughout myogenic differentiation but their localization did. In particular, HP1{gamma} relocalization to heterochromatin correlated with MeCP2 presence. Using co-immunoprecipitation assays, we found that these heterochromatic factors interact in vivo via the chromo shadow domain of HP1 and the first 55 amino acids of MeCP2. We propose that this dynamic interaction of HP1 and MeCP2 increases their concentration at heterochromatin linking two major gene silencing pathways to stabilize transcriptional repression during differentiation.


Present address: Tanja Hardt, Medical Proteomics Center, Ruhr University, 44801, Germany

Alessandro Brero, Ludwig Maximilians University, Gene Center, 81377 Munich, Germany


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