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. 2011 Jun 21;30(15):3004–3018. doi: 10.1038/emboj.2011.199

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Copyright © 2011, European Molecular Biology Organization

This is an open-access article distributed under the terms of the Creative Commons Attribution Noncommercial Share Alike 3.0 Unported License, which allows readers to alter, transform, or build upon the article and then distribute the resulting work under the same or similar license to this one. The work must be attributed back to the original author and commercial use is not permitted without specific permission.

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HF bulge progeny constitute ectopic SGs. (A–C) Detection of bulge marker CD34 (A), α6-integrin (B, Itga6), BrdU (C) and YFP-labelled keratinocytes in deformed HF structures of A_K15CreER^low/K14ΔNLef1/R26RYFP mice. (D–I) Starting with a cluster of YFP+ keratinocytes within the bulge of deformed HFs 3 days after activation (D), HF bulge-derived progeny localises to ectopic SGs (E, nSG, arrows) and are positive for SCD1 (red) after 5 days following Cre activation (E, F, arrows). Chasing for 36 days results in labelled resident bulge SCs (G, arrow heads) and clonal expansion of bulge progeny in deformed HFs at sites of de novo SGs (H, nSG). A_K15CreER^low/K14ΔNLef1/R26RYFP mice treated with vehicle as control (I). Scale bars, 50 μm.