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. 2013 Jan 4;110(4):1351–1356. doi: 10.1073/pnas.1121312110

Fig. 2.

Fig. 2.

hfSCs after BMP inhibition in vivo switch from quiescence to activation and acquire molecular characteristics resembling the HG. (A–B and CD) At P59, in CONRU HFs, strong P-cadherin staining was restricted to the HG and did not overlap with YFP+ cells in the bulge (arrows). In the bulge of cKORU HFs, P-cadherin staining was expanded and increased with overlapping expression observed by YFP+ cells in both the HG and the bulge (arrows). (I–J and G–H) At P62 in the bulge of cKORU, elevated P-cadherin correlated with YFP activation (arrows), whereas, in the CONRU bulge, P-cadherin staining was absent. (E–F and K–L) At P59 and P62, FACS analysis confirmed increased P-cadherin staining in YFP+ cKORU hfSCs compared with CONRU, respectively. (M) Changes in the pool of HG signature genes in cKORU hfSCs were either up-regulated (red type) or down-regulated (green type). Only three genes characterized in cKORU hfSCs were inversely regulated, namely BMP6, NFATc1, and Col20α1 (marked in blue). (Scale bars: 50 µm.)