Figure 3
Figure 3. Histone modifications within the β-globin locus in the absence of the LCR. ChIP assays were performed using anti-H3Ac and anti-H3K4 dimethyl antibodies in primary cells isolated from wild-type (WT) mice and mice homozygous for deletion of the endogenous β-globin LCR (ΔLCR). The β-globin locus and positions of PCR amplimers are shown to scale at the top. Enrichments in E12.5 embryonic blood for (A) H3Ac and (B) H3K4 dimethyl and in E14.5 fetal liver for (C) H3Ac and (D) H3K4 dimethyl are shown in bar graph format beneath. The more lightly shaded portion of the graph represents the region in which enrichments for the indicated histone modifications were significantly lower than in erythroid cells from wild-type mice.

Histone modifications within the β-globin locus in the absence of the LCR. ChIP assays were performed using anti-H3Ac and anti-H3K4 dimethyl antibodies in primary cells isolated from wild-type (WT) mice and mice homozygous for deletion of the endogenous β-globin LCR (ΔLCR). The β-globin locus and positions of PCR amplimers are shown to scale at the top. Enrichments in E12.5 embryonic blood for (A) H3Ac and (B) H3K4 dimethyl and in E14.5 fetal liver for (C) H3Ac and (D) H3K4 dimethyl are shown in bar graph format beneath. The more lightly shaded portion of the graph represents the region in which enrichments for the indicated histone modifications were significantly lower than in erythroid cells from wild-type mice.

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