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. 2016 Jul 1;143(13):2376–2388. doi: 10.1242/dev.137984

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© 2016. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 3. — SOX2 regulates SIX6 expression exclusively in the SOX2^Hi progenitor population. (A) Immunofluorescence for SOX2 and SIX6 at 18.5 dpc in a control embryo. SOX2 is highly expressed in cells lining the pituitary lumen (SOX2^Hi; arrowhead), and at lower levels in cells within IL (SOX2^Low; arrow). Both SOX2-positive cell populations uniformly express SIX6. (B) Immunofluorescence for SOX2 and POMC at 18.5 dpc in a control embryo. SOX2^Low cells are POMC-positive melanotrophs (arrow). (C) Immunofluorescence for SOX2, SIX6 and eYFP in a Pomc-Cre;Sox2^fl/fl;R26R^eYFP/+ embryo at 18.5 dpc. SOX2^Low expression is specifically lost in eYFP-positive melanotrophs, whereas eYFP-negative, SOX2^Hi cells are maintained around the cleft. SIX6 expression in IL is unaffected by the loss of SOX2. (D) Immunofluorescence for SOX2, SIX6 and E-cadherin in Sox2^fl/+;Sox9^CreErt2/+ and Sox2^fl/fl;Sox9^CreErt2/+ embryos at 18.5 dpc, induced by tamoxifen at 13.5 dpc. SOX2 expression is lost in some E-cadherin-positive cells in the epithelial cell layer lining the cleft. Deletion of SOX2 does not result in downregulation of SIX6. Scale bar: 10 μm in A,B,D; 5 μm in C. IL is outlined.