The hairless hr mutation


A mutation in the thyroid hormone pathway in mice and humans: the hairless locus (hr)

NOTE: a mutation in the hairless gene on chromosome 15 has not been found in rats (Ahearn et al. 2002). The hairlessness of rats is caused by other mutations that affect hair production: fuzzy, shorn, and nude (see Coat Types on this site, and The Genotypes of Recessive Hairlessness, by LM Hua for more on these three genes). The Charles River "hairless" rat which is frequenly used in research is a different mutation, an allele of fuzzy (Ahearn et al. 2002, Panteleyev and Christiano 2001).

The hairless mutation has, however, been found in humans and mice, so I am including a brief discussion of it here.

The hairless gene is triggered by thyroid hormone. When stimulated by thyroid hormone, it codes for a corepressor, a factor that facilitates the ability of thyroid hormone to turn off the expression of certain genes. Specifically, it represses the transcription of thyroid hormone receptors. Therefore, when there is no thyroid hormone around, the hairless protein reduces the number of thyroid hormone receptors, which turns off functions that depend on thyroid hormone, including some hair growth factors. As both a thyroid-hormone responsive gene and corepressor for thyroid hormone receptors, hairless is a key mediator of thyroid hormone action in the brain and skin (Potter et al. 2001, Potter et al. 2002).

Hairless is part of the communication system between the thyroid and skin cells. Depending on how serious the mutation in the hairless gene is, the consequences range from patchy to complete hair loss.

Both the hairless (hr) and rhino (hr-rh) mutations are alleles at this locus in the mouse.

Human analogue: There are at least two analogues of hairless in humans: alopecia universalis "universal hairlessness" (Ahmad et al. 1998), and papular atricia (hair loss accompanied by the formation of comedones) (Ahmad et al. 1999a and Ahmad et al. 1999b).

More sites on hairless:

See also Panelelev et al 1998, Panteleyev et al. 2000, Klein et al. 2002.

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