Fig. 2: MCL‑1 is essential for murine HF during adulthood.

A, B Deletion of Mcl‑1 in the skin epithelium leads to progressive hair loss and HF destruction. Representative photographs of Mcl‑1^f/f or Mcl‑1^f/+, K5‑Cre/Mcl‑1^f/+ and K5‑Cre/Mcl‑1^f/f mice at p12, p29, p60 and p90 (A), alongside H&E sections of dorsal skin at these time points (B). Data represent n = 8 mice per genotype. Scale bars, 100 µm. C Representative FACS plots demonstrating efficient deletion of the floxed Mcl‑1 gene, using hCD4 as an indicator of efficient CRE‑mediated recombination as well as promoter activity. Expression of hCD4 in hair bulge (CD49f⁺/CD34⁺/SCA‑1^–), non‑bulge HF cells (CD49f⁺/ CD34^–/SCA‑1^–) and interfollicular epidermis (IFE) (CD49f⁺/CD34^–/SCA‑1⁺) from Mcl‑1^f/f or Mcl‑1^f/+, K5‑Cre/Mcl‑1^f/+ and K5‑Cre/Mcl‑1^f/f mice. n = 3 at p21 per genotype. D qPCR analysis reveals a significant reduction in Mcl‑1 transcript levels in HF cells (CD49f⁺/SCA‑1^–) and IFE (CD49f⁺/SCA‑1⁺), but not in non‑epithelial cells (CD49f^–) of K5‑Cre/Mcl‑1^f/f mice at p21, compared to control littermates. Data are presented as mean of three technical replicates for each point from two independent litters. E Representative confocal images show the absence of MCL‑1 protein in HFs of K5‑Cre/Mcl‑1^f/f mice compared to K5‑Cre/Mcl‑1^f/+ and Mcl‑1^f/f or Mcl‑1 ^f/+ littermate controls at p29 (mid anagen). Data represents n = 5 experiments. Scale bar, 50 µm. F Mcl‑1 deletion leads to apoptosis in HFs, as shown by CC3 staining at various stages: telogen (p60), early anagen (p22), mid anagen (p29), and catagen (p40), representative of n = 5 independent mice per genotype. Basal skin is marked by KRT14, hair matrix with TACs is stained with PCAD, and DAPI is used as nuclear counterstain. Scale bar, 50 µm. G Quantification of CC3⁺ cells per HF at p29 shows significantly increased apoptosis in K5‑Cre/Mcl‑1^f/+ mice (n = 70) vs. controls (n = 40). Data are presented as mean ± SEM for n = 3 mice per genotype. ****p < 0.0001, Student’s t‑test.