Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 104, Issue 49, Pages 19416-19421Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0707442104
Keywords
chromatin; DNA methylation; epigenetics; genomics; Rett syndrome
Categories
Funding
- NCRR NIH HHS [C06 RR12088, C06 RR012088] Funding Source: Medline
- NICHD NIH HHS [R01 HD048799, R01 HD/NS41462, R01 HD041462-04, R01 HD048799-03, R01 HD041462, R01 HD041462-05] Funding Source: Medline
- NINDS NIH HHS [R01 NS041462] Funding Source: Medline
Ask authors/readers for more resources
Mutations in MECP2 cause the autism-spectrum disorder Rett syndrome. MeCP2 is predicted to bind to methylated promoters and silence transcription. However, the first large-scale mapping of neuronal MeCP2-binding sites on 26.3 Mb of imprinted and non-imprinted loci revealed that 59% of MeCP2-binding sites are outside of genes and that only 6% are in CpG islands. Integrated genome-wide promoter analysis of MeCP2 binding, CpG methylation, and gene expression revealed that 63% of MeCP2-bound promoters are actively expressed and that only 6% are highly methylated. These results indicate that the primary function of MeCP2 is not the silencing of methylated promoters.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available