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. Author manuscript; available in PMC: 2021 Jan 10.
Published in final edited form as: Science. 2019 Dec 19;367(6474):161–166. doi: 10.1126/science.aax9131

Fig. 3. The dermal sheath functionally contracts and is required for regression in vivo.

Fig. 3.

(A) Schematic of live imaging microdissected follicles pre-incubated with or without MLCK inhibitor ML7 and after high K+ depolarization. (B, C) Still images from brightfield movie at start (black) and end (pink) of high K+ incubation. Overlays highlight reduction of follicle width, blocked by ML7. (D) Quantification of follicle widths during live imaging. n = 7 follicles for ML7 and no inhibitor pre-incubation. Data points are mean ± s.d. **P < 0.01, unpaired two-tailed t-test. (E-G) Topical inhibition of MLCK by ML7 blocks hair follicle regression in vivo. Schematic of ML7 or vehicle application during catagen (E). Whole mount IF of P20 back skins show normal regression of follicles into telogen rest in control, but stalled follicles in contraction-inhibited ML7-treated regions (F). (G) Quantification of % stalled follicles (n = 1071 control, n = 1019 ML7-treated; 10 mice). Data bars are mean ± s.d. **P = 0.001, unpaired two-tailed t-test. (H) IF for LEF1, Ki67, αSMA and K14. Stalled follicles have intact DS (αSMA) and DP (LEF1) that are no longer engulfed. Epithelial cells (K14) of stalled follicles are not proliferative (Ki67). Scale bars, 50 μm (B, C, F) and 10 μm (H).