Mouse model of alopecia

Scientists have developed a mouse model of inherited baldness, which they anticipate will further the current understanding of the molecular mechanisms underlying human hair loss.

The report is published in the June 1 issue of the scientific journal Genes & Development.

Dr. Pierre Coulombe and colleagues at Johns Hopkins School of Medicine (Maryland) and the CNRS-Institut Pasteur (France) have genetically engineered mice to lack a gene that encodes a keratin protein. Keratins are structural proteins found in all epithelia including the hair, nails and epidermis of humans, as well as the fur, feathers and hooves of animals. Of the nearly thirty keratin genes expressed in hair follicles, Dr. Coulombe and colleagues found that a deficiency in just one keratin 17 causes temporary baldness in mice.

Dr. Coulombe and colleagues generated keratin 17 (K17)-deficient mice, or K17 knockout mice, in order to define the function of the keratin 17 protein. They found that K17 knockout mice appear normal at birth, but within a few days display a peculiar hair phenotype. Whereas normal newborn mice develop their characteristic fur coat within 3-7 days after birth, a portion of newborn K17-deficient mice do not grow fur at all within the first few weeks of their lives.

Dr. Coulombe and colleagues determined that the cause of alopecia, or baldness, in these K17 knockout mice is severe hair fragility and premature death of hair-producing cells, thereby establishing keratin 17 as a crucial factor in the normal emergence of hair early after birth. Although the severity of alopecia was variable in the K17 knockout mice, one key featured emerged: Regardless of how severely afflicted the K17-deficient mice were, at about three weeks old, all of the mice began to grow fur.

The researchers noted that this dramatic change correlates with the beginning of a new, postnatal hair growth cycle, suggesting that keratin 17 activity becomes less crucial in

Contact: Heather Cosel
Cold Spring Harbor Laboratory

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