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. 2011 Jul 15;355(2-2):372–380. doi: 10.1016/j.ydbio.2011.04.005

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© 2011 Elsevier Inc.

Open Access under CC BY 3.0 license

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Fig. 4 — Transgenic mutation analysis shows that BS-1 is essential for enhancer function. (A) Mutation of the putative BS-4, BS-5 and BS-6 binding sites (construct ECR111[m456]-MZ) does not interfere with ECR111 activity at 10.5 dpc. (B) The ECR111-BE-MZ construct drives expression in the brain (arrowhead) and the somitic ECR111 domain. (C) Mutation of BS-1, BS-2 and BS-3 binding sites (construct ECR111[m123]-BE-MZ) or (D) the single mutation of BS-1, abolish ECR111-driven expression at 10.5 dpc, but not that driven by the brain element (BE) used as a transgenesis expression control (arrowheads in C and D).