Fig. 6. Laminin 5 and entactin are disorganised in adult 3-integrin-deficient interfollicular but not follicular epidermis. WT (A,D,G) and 3-integrin-deficient (B,C,E,F,H,I) adult skin grafts were analysed by immunofluorescence with antibodies to Lm-5 (A-C), entactin (D-F) and Coll IV (G-I). In WT skin grafts, Lm-5, entactin and Coll IV were localised in the basement membrane zone of the interfollicular and follicular epidermis (A,D,G, respectively). In contrast, in 3-integrin-deficient skin Lm-5 and entactin appeared disorganised at the dermal-epidermal junction of the interfollicular epidermis but not in the basement membrane of normal hair follicles (B and E, respectively) or hair follicle clusters (C and F, respectively). The distribution of Coll IV was not affected in 3-integrin-deficient skin samples in either the interfollicular or follicular compartments (H,I). 11-15 skin grafts for each genotype were analysed and the experiment was repeated three times. Over 500 follicles per genotype were analysed. Electron micrographs of interfollicular epidermis of adult WT (J) and 3-integrin-deficient (K,L) skin grafts. The epidermis appeared to stratify normally, and hemidesmosomes were evident in both WT and 3-integrin-deficient samples. Note that the lamina densa is disrupted between hemidesmosomes. For electron microscopy, four skin grafts per genotype were analysed. Arrows, basement membrane zone; arrowheads, disorganised basement membrane; b, basal layer; s, spinous layer; c, cornified layer; HD, hemidesmosomes; LD, lamina densa; empty arrowheads, interrupted lamina densa. Bar represents 50 µm in A-I; 1 µm in J and K, 200 nm in L.

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