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. 2002 Apr 30;99(10):6816–6821. doi: 10.1073/pnas.092130099

Figure 4.

Figure 4

Cleavage at the dermal side of the cutaneous BMZ is responsible for skin blistering in GRIP1−/− mutants. (A) Hematoxylin-eosin-stained sections of lower limbs of wt (a and b) and GRIP1−/− (c and d) E12 embryos. Serous blisters are clearly visible on both sides of the limb (c). At higher magnification, the epidermis appears diffusely detached from the underlying dermis in blistered (arrowhead) and nonblistered areas (arrow). (B) Immunostaining of limb sections of wt (a–c) and GRIP1−/− (d–f) E12 embryos with antibodies recognizing laminin (a and d), collagen type VII (b and e), and PECAM (c and f; counterstaining with Hoechst 33258). Laminin staining segregates on the roof of the bulla (d, arrowheads), whereas collagen type VII is present on both sides of the tissue cleft (e, arrowheads). (Magnifications: A a and c, ×20, b and d, ×60; B, a–f, ×60.)