Fig. 5.

Phenotype of the homozygous knockout mice. (A) RT-PCR analysis of RNA samples from the lungs (L) and kidneys (K) of the WT and homozygous knockout mice. Homozygous knockout offspring lack expression of occludin mRNA (624-bp fragment). (B) Western blot analysis with anti-occludin polyclonal antibody of samples from the lungs and kidneys of the WT and homozygous knockout mice. The occludin protein (≈66 kDa) is absent in the homozygous knockout mouse. (C and D) Histological analysis of the salivary glands of 6-week-old WT (C) and homozygous (D) mice produced by gene targeting, showing a loss of cytoplasmic granules in the mutant, which can be found in the WT (C, arrow). (E–G) Histological analysis of the gastric mucosa of 4-week-old WT (E) and homozygous (F and G) mice produced by gene trapping. The predominant hyperplasia of the foveolar cells (F, arrow) is accompanied by a significant loss of chief and parietal cells and the degeneration of the proper muscle of the stomach with chronic inflammation (F, arrowhead). Infiltration of neutrophils and lymphocytes is widely apparent (G, arrow). Similar histology was found in the homozygous mutant made by gene targeting. (H and I) Histological analysis of the femoral bones of 6-week-old WT (H) and homozygous (I) mice produced by gene targeting. Trabecular development is decreased in the mutant. Hematoxylin and eosin staining was used. (Scale bars: C–I, 100 μm.)