Figure 6
Figure 6. PcG-regulation at the HBA genes in human ES cells. (A) ChIP experiments carried out in human ES cells using antibodies against SUZ12 (top panel) or H3K27me3 (bottom panel). Immunoprecipitated material was analyzed at amplicons surrounding the α-globin locus (Figure 1) or at the β-globin gene promoter, 3′ of the β-globin gene, within HS5 of the β-globin locus control region (probes HBB ex1, 3′HBB, and βLCR HS5) or a control amplicon within the 18S rRNA gene. Data indicate the percentage of input material precipitated at each amplicon. (B) Real-time RT-PCR analysis of HBA2 cDNA in human ES cells which were either mock-treated, or treated with 0.2 μmol/L TSA for 8 hours. Results are shown as fold change relative to mock-treated cells after normalizing for GAPDH signal. Data in panels A and B show the mean values obtained from replicate experiments with error bars indicating the range of values.

PcG-regulation at the HBA genes in human ES cells. (A) ChIP experiments carried out in human ES cells using antibodies against SUZ12 (top panel) or H3K27me3 (bottom panel). Immunoprecipitated material was analyzed at amplicons surrounding the α-globin locus (Figure 1) or at the β-globin gene promoter, 3′ of the β-globin gene, within HS5 of the β-globin locus control region (probes HBB ex1, 3′HBB, and βLCR HS5) or a control amplicon within the 18S rRNA gene. Data indicate the percentage of input material precipitated at each amplicon. (B) Real-time RT-PCR analysis of HBA2 cDNA in human ES cells which were either mock-treated, or treated with 0.2 μmol/L TSA for 8 hours. Results are shown as fold change relative to mock-treated cells after normalizing for GAPDH signal. Data in panels A and B show the mean values obtained from replicate experiments with error bars indicating the range of values.

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