Disruption of DNA-methylation-dependent long gene repression in Rett syndrome View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-06

AUTHORS

Harrison W. Gabel, Benyam Kinde, Hume Stroud, Caitlin S. Gilbert, David A. Harmin, Nathaniel R. Kastan, Martin Hemberg, Daniel H. Ebert, Michael E. Greenberg

ABSTRACT

Disruption of the MECP2 gene leads to Rett syndrome (RTT), a severe neurological disorder with features of autism. MECP2 encodes a methyl-DNA-binding protein that has been proposed to function as a transcriptional repressor, but despite numerous mouse studies examining neuronal gene expression in Mecp2 mutants, no clear model has emerged for how MeCP2 protein regulates transcription. Here we identify a genome-wide length-dependent increase in gene expression in MeCP2 mutant mouse models and human RTT brains. We present evidence that MeCP2 represses gene expression by binding to methylated CA sites within long genes, and that in neurons lacking MeCP2, decreasing the expression of long genes attenuates RTT-associated cellular deficits. In addition, we find that long genes as a population are enriched for neuronal functions and selectively expressed in the brain. These findings suggest that mutations in MeCP2 may cause neurological dysfunction by specifically disrupting long gene expression in the brain. More... »

PAGES

89

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature14319

    DOI

    http://dx.doi.org/10.1038/nature14319

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1015767010

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/25762136


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