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Vol. 11, Issue 12, 4131-4142, December 2000
¶¶ and
*Department of Cell Biology, Kyoto University Faculty of Medicine,
Sakyo-ku, Kyoto 606-8501, Japan; Occludin is an integral membrane protein with four transmembrane
domains that is exclusively localized at tight junction (TJ) strands.
Here, we describe the generation and analysis of mice carrying a null
mutation in the occludin gene. Occludin KAN Research Institute
Inc., Kyoto Research Park, Chudoji, Shimogyo-ku, Kyoto 600-8317, Japan;
Medizinische Klinik I Gastroenterologie und
Infektiologie and §Institut für Klinische
Physiologie, Universitätsklinikum Benjamin Franklin, Freie
Universität Berlin, Berlin, Germany; Department of
Cell Biology, Cancer Institute, Toshima-ku, Tokyo 170-8455, Japan; and
¶Department of Molecular Genetics, Tohoku University
School of Medicine, Sendai 980-8575, Japan
/ mice were born with no
gross phenotype in the expected Mendelian ratios, but they showed
significant postnatal growth retardation. Occludin / males produced
no litters with wild-type females, whereas occludin / females
produced litters normally when mated with wild-type males but did not
suckle them. In occludin / mice, TJs themselves did not appear to
be affected morphologically, and the barrier function of intestinal
epithelium was normal as far as examined electrophysiologically.
However, histological abnormalities were found in several tissues,
i.e., chronic inflammation and hyperplasia of the gastric epithelium,
calcification in the brain, testicular atrophy, loss of cytoplasmic
granules in striated duct cells of the salivary gland, and thinning of
the compact bone. These phenotypes suggested that the functions of TJs
as well as occludin are more complex than previously supposed.
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