Figure EV3. Mutant^GFP bulge HF‐SCs are active and initiate psoriasis‐like development (related to Fig 3).

• A
  Immunofluorescence images of the ears of control (Co) and DKO* mice showing co‐expression of mutant^GFP with CD34 (red arrows) in HF‐SCs. n = 3. Scale bar = 50 μm.
• B, C
  Gene expression of quiescence transcription factors, Foxc1a and Nfatc1 show that HF‐SCs exit the quiescent stage during psoriasis‐like development in DKO* mice. n = 3 mice per group. Data represent mean ± SD. Statistical significance ***P < 0.001 (Student's two‐tailed t‐test relative to control group). See Appendix Table S2 for exact P‐values.
• D
  Colony formation in vitro of bulge hair follicle stem cells (HF‐SCs, CD34⁺ CD49f^high) vs. basal keratinocytes (b‐KCs, CD49f^high) from control and DKO*‐mT/mG ears shows that mutant^GFP HF‐SCs have significant increased colony formation when compared to non‐mutant^Tom HF‐SCs or control HF‐SCs. n = 3 mice per group. Data represent mean ± SD. Statistical significance **P < 0.01 (Student's two‐tailed t‐test relative to control groups). See Appendix Table S2 for exact P‐values.
• E
  Representative images of whole mount of ear skin from DKO*^K15‐mT/mG at day 0 after mifepristone treatment in two views from the epidermis and from the dermis, to distinguish the expression of GFP⁺ epidermal cell in IFE and HFs.
• F
  Immunofluorescence images of c‐Jun and JunB staining in DKO* ^K15‐mT/mG at days 5–7 after tamoxifen treatment show GFP⁺ keratinocytes are negative for c‐Jun and JunB expression.
• G
  Representation of both epidermal lineage‐tracking system, DKO*‐mT/mG and DKO* ^K15‐mT/mG, for investigating the origin and contribution of epidermal stem cells in the development of psoriasis‐like.