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Status |
Public on Mar 31, 2015 |
Title |
Mecp2: an unexpected regulator of macrophage gene expression and function [ChIP-Seq] |
Organism |
Mus musculus |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
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.
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Overall design |
Examination of NCOR2 and HDAC3 genome-wide location in bone-marrow derived macrophages.
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Contributor(s) |
Litvak V |
Citation(s) |
25902482 |
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Submission date |
Mar 04, 2015 |
Last update date |
May 15, 2019 |
Contact name |
Stephen Turner |
Organization name |
Signature Science, LLC
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Street address |
1670 Discovery Drive
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City |
Charlottesville |
State/province |
VA |
ZIP/Postal code |
22911 |
Country |
USA |
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Platforms (1) |
GPL13112 |
Illumina HiSeq 2000 (Mus musculus) |
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Samples (2) |
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This SubSeries is part of SuperSeries: |
GSE66502 |
Mecp2: an unexpected regulator of macrophage gene expression and function |
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Relations |
BioProject |
PRJNA277172 |
SRA |
SRP055805 |