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J. Cell Biol.,
Volume 143, Number 2, October 19, 1998 487-499
* Howard Hughes Medical Institute, Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago,
IL 60637; and Dividing populations of stratified and simple
epithelial tissues express keratins 5 and 14, and keratins
8 and 18, respectively. It has been suggested that these
keratins form a mechanical framework important to
cellular integrity, since their absence gives rise to a blistering skin disorder in neonatal epidermis, and hemorrhaging within the embryonic liver. An unresolved fundamental issue is whether different keratins perform
unique functions in epithelia. We now address this
question using transgenic technology to express a K16-14 hybrid epidermal keratin transgene and a K18 simple epithelial keratin transgene in the epidermis of mice
null for K14. Under conditions where the hybrid epidermal keratin restored a wild-type phenotype to newborn epidermis, K18 partially but not fully rescued. The
explanation does not appear to reside in an inability of
K18 to form 10-nm filaments with K5, which it does in
vitro and in vivo. Rather, it appears that the keratin
network formed between K5 and K18 is deficient in
withstanding mechanical stress, leading to perturbations in the keratin network in regions of the skin that
are subjected either to natural or to mechanically induced trauma. Taken together, these findings suggest
that the loss of a type I epidermal keratin cannot be
fully compensated by its counterpart of simple epithelial cells, and that in vivo, all keratins are not equivalent.
Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205
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