Chromatin context and ncRNA highlight targets of MeCP2 in brain

摘要: The discovery that Rett syndrome (RTT) is caused by mutation of the methyl-CpG-binding-protein MeCP2 provided a major breakthrough in understanding neurodevelopmental disorder and accelerated research. However, gene regulation complicated. current consensus for remains as classical repressor complex, with emphasis on its role methylation-dependent binding repression. recent evidence indicates additional regulatory roles, suggesting non-classical mechanisms activation. This has opened field research suggests targets may not be usual suspects, is, dependent only DNA methylation. Here we examine how chromatin sequence preference confer functionality, connect relevant pathways an active genome. Finding both genomic proteomic to indicate spliceosome interaction, consequently discovered broad enrichment transcriptome while our focus toward long non-coding RNA (lncRNA) revealed association RNCR3. Our data as-yet-unappreciated between lncRNA MeCP2. We hypothesize ncRNA mediate chromatin-remodeling events interacting MeCP2, thereby conferring changes expression. consider these results suggest new conferred interactions upon structure function.