Temporary Baldness Traced to Gene Malfunction

Working with a mouse model that closely resembles human hereditary baldness, researchers have found that the keratin 17 gene (K-17) plays a crucial role in temporary hair loss in mice and in ectodermal dysplasia epithelial disorders in humans. These findings were reported in the June 1, 2002, issue of Genes & Development.

Investigators developed a strain of mice lacking keratin-producing gene K-17, one of the nearly 30 keratin genes expressed in hair follicles. Growth of fur in these mice was temporarily disrupted. Whereas normal newborn mice develop their fur coat within three to seven days after birth, some newborn K17-deficient mice do not grow fur at all within the first few weeks of their lives. Other mice demonstrated lesser degrees of hair loss. A closer look revealed that the mice suffered from severe hair fragility and the premature death of hair-producing cells.

In humans inherited mutations in the keratin 17 gene cause two separate epithelial disorders related to ectodermal dysplasias. Although each disorder causes a different epithelial deformity, both share a tendency for hair follicle abnormalities. Furthermore, the hair abnormalities that occur in people with inherited K-17 mutations vary both in frequency and severity--just like those in mice lacking K-17.

As Dr. Pierre Coulombe of the Johns Hopkins School of Medicine (Baltimore, MD, USA) explains, this work represents a marked advance because "not only are the features of these mice very informative with regards to how hair tissue works and the role of keratin proteins in hair structure and growth, it also provides significant insight into the clinical heterogeneity of the skin diseases arising as a result of inherited mutations in the keratin 17 gene.” The research was conducted by Dr. Coulombe and colleagues at Johns Hopkins and the CNRS-Institut Pasteur (Paris, France).



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Johns Hopkins University
Institut Pasteur