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

Figure EV1. Bcl‐2 inhibition causes SC‐specific cell death and loss of suprabasal BSCs.

Figure EV1

  1. Schematic of the hair cycle phases anagen (growth), catagen (regression) and telogen (rest).
  2. HF Schematic focusing on basal and suprabasal bulge SCs (bBSCs, sbBSCs), the hair germ (HG) and the dermal papilla (DP). IFE, interfollicular epidermis; SG, sebaceous glands.
  3. Timeline experimental ABT‐199 treatment (P50) and analysis (P51) in telogen and Immunofluorescence staining of telogen tail whole mounts for Keratin 15 (Krt15) and active caspase‐3 (aCas3) in control (Ctr) and Bcl‐2 inhibitor (ABT‐199)‐treated mice. B, bulge; HF, hair follicle; SG, sebaceous gland; dashed lines, sebaceous glands. Scale bar, 100 µm.
  4. Quantification of tail HF with aCas3+ cells in bulge and hair germ of control (Ctr) and ABT‐199‐treated mice (n = 4 biological replicates; mean ± standard deviation (SD); ***P < 0.001, ns=not significant, two‐tailed unpaired Student's t‐test.
  5. Immunofluorescence staining of telogen tail whole mounts for tyrosinase‐related protein‐2 (Trp2) in wild‐type (wt) animals (n = 3 mice). SG, sebaceous gland; B, bulge; HG: hair germ; dashed lines: sebaceous glands. Scale bar, 100 µm.
  6. Model for Bcl‐2‐mediated protection of suprabasal BSCs from apoptosis.