Fig. 5

Phenotypic changes in skin of NCSTN gene knockout mice; the skin lesions include shedding hair, recurrent inflammatory papules, plaques, pustules, cysts, ulcer, and scars. The above skin lesions are mainly concentrated in the posterior neck (a1), back (a2, a3, a4), groin (b2–b4), axilla (b4), and mouth and nose (a2) (as shown by yellow arrows). b1–b4 show the changes in skin phenotypes over time in the same NCSTN gene knockout mice without tamoxifen (b1) and after tamoxifen injection (b2–b4). The observation time of the skin phenotype was recorded after induction of NCSTN gene knockout mice with tamoxifen (b2 > 6 weeks, b3 > 10 weeks, b4 > 6 months) (as shown by the yellow arrow). c1–d6: Microscopic features of skin in wild type and NCSTN gene knockout mice; c1 and c2 are pathological manifestations of skin in wild-type mice (c1 × 100; c2 × 400). Compared with the microstructure of skin tissue in wild-type mice, NCSTN gene knockout mice show epidermal thickening (d2 × 100, d3 × 100), increased inflammatory cells (d2 × 100, d3 × 100), keratosis of hair follicles (d2 × 100, d4 × 100, d5 × 400), fewer hair follicles (d1 × 100, d2 × 100), and full-layer loss of epidermis in severe cases (d1 × 100, d6 × 400). These skin manifestations are shown by yellow arrows. e Relationship between sex (male VS female) and skin lesion phenotype in NCSTN gene knockout mice by Fisher's exact test, P < 0.05. This result shows that the sex of mice correlates with skin lesion (+ : skin lesions; −: normal)