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. 2013 Jan 10;24(5):1361–1372. doi: 10.1093/cercor/bhs421

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© The Author 2013. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial 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 6. — Critical period for Lhx2 to regulate the forebrain hem system ends by E10.5. Conditional deletion of Lhx2 using a tamoxifen-inducible CreER driver. Tamoxifen administration at E10.5 (T10.5) does not interfere with forebrain development in control (CreER;Lhx2lox/+) embryos (A–I). A probe against Lhx2 exon 2,3 indicates that Lhx2 deletion has occurred throughout the brain of the floxed (CreER;Lhx2lox/−) embryos (C, F, I). (A–C) The septum in the floxed embryos appears normal as evident from Six3 and Fgf17 expression (bars; A and B). (D and E) Thalamic eminence expressing Mab21l2 and Tbr1 appear similar in the floxed embryos as that in controls (asterisk). Similarly, expression of Wnt8b in the cortical hem, medial pallium, and thalamic eminence as well as of Wnt3a in the cortical hem is comparable between floxed and control embryos (G and H). Scale bar: 300 µm.