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. 2021 Aug 2;22(10):e52301. doi: 10.15252/embr.202052301

Figure 1. Differential requirement for Bcl‐2 preventing suprabasal BSC loss.

Figure 1

  • A
    Treatment scheme of experimental timeline and Immunofluorescence staining of telogen back skin hair follicles (HF) for Integrin α6 (Itgα6, red), active caspase‐3 (aCas3, green) and DAPI (blue) in control (Ctr) and Bcl‐2 inhibitor (ABT‐199)‐treated mice. B, bulge; CH, club hair; DP, dermal papilla; HF, hair follicle; HG, secondary hair germ. Scale bar, 50 µm.
  • B
    Quantification of back skin HF with aCas3+ cells in bulge, hair germ and dermal papilla of Ctr and ABT‐199‐treated mice (n = 4 mice biological replicates; mean ± standard deviation (SD); ***P < 0.001, ns, not significant, two‐way ANOVA test). nd, not detected.
  • C, D
    Treatment scheme, FACS plot (C) and quantification (D) of keratinocytes stained for CD34 and Itgα6 after 6 days of treatment with vehicle solution (Ctr) or ABT‐199 (n = 6 biological replicates; mean ± standard deviation [SD]; **P < 0.01, ns = not significant, two‐tailed unpaired Student's t‐test). suprabasal (sbBSC, CD34+/Itgα6low), basal (bBSC, CD34+/Itgα6high) BSCs and n‐B (non‐bulge epidermal cells). **P < 0.005.