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. 2017 Aug 22;8(42):72363–72374. doi: 10.18632/oncotarget.20390

Figure 3. H19/Igf2 imprinting methylation statuses and transcription and the expression of genes regulating imprinting methylation in PFFs and cloned embryos and the cloned blastocysts derived from PFFs treated with 5-aza-dC.

Figure 3

(A) the methylation statuses of H19/Igf2 imprinting in PFFs treated with 5-aza-dC, (B) the methylation statuses of H19/Igf2 imprinting at the 4-cell and blastocyst stages of cloned embryos derived from PFFs treated with 5-aza-dC, (C) the transcription of H19/Igf2 and genes regulating imprinting methylation at the 4-cell and blastocyst stages of cloned embryos derived from PFFs treated with 5-aza-dC, (D) the cloned blastocysts derived from PFFs treated with 5-aza-dC (Scale bar = 500 μm). Treating donor cells with 5-aza-dC resulted in the hypomethylated H19/Igf2 imprinting in PFFs and cloned embryos, disrupted H19 transcription, reduced expression of Igf2 and genes regulating imprinting methylation and downregulated blastocyst rate. Aza (+) and Aza (−) represented PFFs treated with 5-aza-dC or not. Black or white circles indicate methylated or unmethylated CpG sites, respectively. a–bValues for a given gene with different superscripts differ significantly (P < 0.05).