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A new mouse for studying baldness and how wounds heal


Scientists have developed a laboratory mouse that is bald during its first weeks of life and can be used to investigate the healing of wounds. The mouse lacks the protein keratin 17, which is essential for hair growth after birth and also plays a role in the skin's response to injury. The mouse grows hair a few weeks after birth, presumably because different genes are involved in 'adult' hair and because related genes compensate for the missing keratin 17.

Mouse lacking keratin 17 (left) and normal mouse.

Keratins are structural proteins found in different types of cells, including hair, nails, and skin cells. Mutations in these genes cause skin and related diseases in humans; there are dozens of known human keratin proteins.

Giving the severity of the baldness effect on the mice, it was surprising that the mice did not also have defects in their nails or other appendages, says Pierre A. Coulombe, of the Johns Hopkins School of Medicine in Baltimore, who led the study. The baldness is in part due to the premature death of cells that produce hair.

Once the adult hair cycle begins, two other mouse keratins (14 and 16) are activated to compensate for the defect. The researchers report that non-keratin genes play a role in compensating for the defect, illustrating the complex genetics of the hair-growth cycle in mammals. The findings are published in Genes and Development.

The researchers created the mouse to investigate the function of keratin 17 proteins in helping wounds to heal. Based on preliminary findings, they conclude that keratin 17 in mice is important for repairing wounds in the embryo.

"We know of about fifty keratin genes in humans, and there's something special about keratin 17," says Coulombe, who collaborated on the project with researchers at the CNRS-Institut Pasteur in Paris. "By understanding its function we might be able to make a contribution to understanding the biology of hair."

The new mouse is not a model of any specific keratin disease in humans. But it may help resolve a puzzle: Humans born with defects in the keratin 17 gene develop two distinct disorders—one primarily affects the sebaceous glands, the other the nails. Both can affect hair as well.

Genetic differences among individuals may be the reason why apparently different diseases can result from keratin 17 mutations: Some persons naturally do a better job compensating for missing keratin than others. Researchers can now investigate this question using the mouse model.

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McGowan, K.M. et al. Keratin 17 null mice exhibit age- and strain-dependent alopecia. Genes Dev 16, 1412-1422 (June 1, 2002).

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