Fig. 3: Allele-specific chromatin state of 15q11.2-q13 region that was not affected by EHMT2 and DNA methylation inhibitors.
From: Mechanism of EHMT2-mediated genomic imprinting associated with Prader-Willi syndrome
a Genome viewer screenshot of ATAC-seq analysis illustrating a closed chromatin state of maternal imprinting domains (PWS) and an open chromatin state of paternal imprinting domains (AS). The control (Ctr) also shows an open chromatin state. b ChIP–qPCR quantification of H3K9me2 on the upstream region of SNRPN gene (§, ATAC-seq peak) in human fibroblasts derived from Angelman syndrome (AS) and PWS patients with a 15q11.2-q13 deletion (One-way ANOVA test followed by Dunnett’s multiple comparison test; Adj p-value is indicated in graph; 50th percentile (median value, line), 25th to 75th percentiles of dataset (box), 5th and 95th percentile (Whiskers). c Genome viewer screenshot illustrating maternal imprinting domains (PWS) remain to be a closed chromatin after treatment of MS1262 (EHMT2 inhibitor) or 5-Aza (DNMT1 inhibitor). d Genome viewer screenshot demonstrating Ehmt2 catalytic mutant (CM) or Ehmt2/Ehmt1 double knockout (DKO) not contributing to open chromatin status on PWS-IC in mouse embryonic stem cells (ESC). Source data are provided as a Source Data file.
