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MBC in Press, published online ahead of print October 15, 2008
Mol. Biol. Cell 10.1091/mbc.E08-05-0510

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Submitted on May 22, 2008
Revised on September 26, 2008
Accepted on October 3, 2008

Disruption of the Interaction between TIF1{beta} and HP1 Leads to a Switch from DNA Hyper- to Hypomethylation and H3K9 to H3K27 Trimethylation on the MEST Promoter Correlating with Gene Reactivation

Raphaël Riclet,* Mariam Chendeb,* Jean-Luc Vonesch,* Dirk Koczan,{dagger} Hans-Juergen Thiesen,{dagger} Régine Losson,* and Florence Cammas*

*Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP/Collège de France, 67404 Illkirch-Cedex, France; {dagger}Institute for Immunology, Medical Faculty, 18057 Rostock, Germany

Monitoring Editor: Wendy Bickmore

Here we identified the imprinted Mesoderm Specific Transcript (MEST) gene as an endogenous TIF1{beta} primary target gene and demonstrated that TIF1{beta}, through its interaction with HP1, is essential in establishing and maintaining a local heterochromatin-like structure on MEST promoter region characterized by H3K9 trimethylation and hypoacetylation, H4K20 trimethylation, DNA hypermethylation and enrichment in HP1, that correlates with preferential association to foci of pericentromeric heterochromatin and transcriptional repression. On disruption of the interaction between TIF1{beta} and HP1, TIF1{beta} is released from the promoter region and there is a switch from DNA hypermethylation and histone H3K9 trimethylation to DNA hypomethylation and histone H3K27 trimethylation correlating with rapid reactivation of MEST expression. Interestingly, we provide evidence that the imprinted MEST allele DNA methylation is insensitive to TIF1{beta} loss of function, whereas the nonimprinted allele is regulated through a distinct TIF1{beta}-DNA methylation mechanism.

Address correspondence to: Régine Losson (losson{at}igbmc.u-strasbg.fr)




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