Mecp2: an unexpected regulator of macrophage gene expression and function [ChIP-Seq]
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ABSTRACT: Mutations in methyl-CpG-binding protein 2 (MeCP2), a major epigenetic regulator, are the predominant cause of Rett syndrome. We previously found that Mecp2-null microglia are deficient in phagocytic ability, and that engraftment of wild-type monocytes into the brain of Mecp2-deficient mice attenuates pathology. We have observed that Mecp2 deficiency is associated with increased levels of histone acetylation at the cis-regulatory regions of the Mecp2-regulated genes in macrophages. We hypothesized that Mecp2 recruits protein complexes containing histone deacetylases (HDACs) to repress the expression of its target genes. Our ChIP-Seq studies in bone-marrow derived macrophages revealed that Mecp2 co-localizes with Ncor2/Hdac3 protein complex at cis-regulatory regions of the target genes. These results suggest a role for Mecp2 in the recruitment and regulation of Ncor2/Hdac3 repressosome that plays a critical role in the regulation of inflammatory responses in macrophages.
ORGANISM(S): Mus musculus
PROVIDER: GSE66501 | GEO | 2015/03/31
SECONDARY ACCESSION(S): PRJNA277172
REPOSITORIES: GEO
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