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. 2016 May 3;44(15):7173–7188. doi: 10.1093/nar/gkw327

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© The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 7. — Loss of Setd1a disrupts enhancer/promoter interactions in the β-globin gene locus. (A) Schematic representation of the 3C fragments after BglII digestion over the mouse β-globin locus. (B and C) 3C analysis of the interaction between the HS2/3 or HS2 enhancer and β-globin promoters in the β-globin locus at day 19 EBs upon Setd1a KD. Data are shown as PCR quantitation of the 3C products. (D) Digestion efficiency of ϵy, βH1, HS2 and βmaj BglII digested sites in the control and Setd1a KD EBs at day 19 of erythroid differentiation, HS4 as a loading control. Data are collected from at least three independent experiments shown as mean ± SEM. *P < 0.05; **P < 0.01 by student t-test.