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Disruption of DNA-methylation-dependent long gene repression in Rett syndrome
Time：Jul 02, 2016 View：
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 a group of scientists at Harvard University identify a genome-wide length-dependent increase in gene expression in MeCP2 mutant mouse models and human RTT brains. They 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, they 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.
Gabel et al. (2015) Nature. doi:10.1038/nature14319.
Gabel et al. (2015) Nature. doi:10.1038/nature14319.
