Genome-wide profiling of histone modification H3K27ac and CTCF transcription factor binding in Rett syndrome iPS cells
Rett syndrome (RTT) is a rare neurodevelopmental disorder that primarily affects females. It is caused by mutations in the MECP2 gene located on the X chromosome, which plays a critical role in normal brain development and function. The mutation induces epigenetic changes and chromatin re-arrangement which lead to alteration to H3K27ac and CTCF binding in the genome. To determine the epigenetic changes in RTT cells, we performed ChIP-seq on healthy and Rett syndrome iPS cells. RTT increased the H3K27ac marks and reduce CTCF binding, which supports the evidence of MeCP2 role in chromatin alterations. Overall design: We performed chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone modification H3K27ac and transcription factor CCCTC-binding factor (CTCF) in both wild-type and MeCP2-mutated (RTT) iPS cells. Two biological replicates were used and the experiments were performed at most three replicates. Peak calling and differential ChIP-seq peak analysis was performed to elucidate the genomic changes occurred in RTT cells.