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doi: 10.1242/10.1242/dev.00201
DEVELOPMENT AND DISEASE |
1 Division of Genetics, Department of Medicine, Brigham and Women's Hospital and
Harvard Medical School, Boston, MA 02115, USA
2 Department of Cell and Molecular Biology, Tulane University, New Orleans, LA
70118, USA
3 Department of Pathology, University of Southern California, Los Angeles, CA
90033, USA
4 Center for Craniofacial Molecular Biology, University of Southern California,
Los Angeles, CA 90033, USA
5 Department of Dermatology, University Hospital Hamburg-Eppendorf, 20246
Hamburg, Germany
6 The Jackson Laboratory, Bar Harbor, ME 04069, USA
7 Department of Biochemistry, University of Southern California, Los Angeles, CA
90033, USA
* Authors for correspondence (e-mail: chuong{at}pathfinder.usc.edu and maas{at}rascal.med.harvard.edu)
Accepted 2 October 2002
Msx2-deficient mice exhibit progressive hair loss, starting at P14 and followed by successive cycles of wavelike regrowth and loss. During the hair cycle, Msx2 deficiency shortens anagen phase, but prolongs catagen and telogen. Msx2-deficient hair shafts are structurally abnormal. Molecular analyses suggest a Bmp4/Bmp2/Msx2/Foxn1 acidic hair keratin pathway is involved. These structurally abnormal hairs are easily dislodged in catagen implying a precocious exogen. Deficiency in Msx2 helps to reveal the distinctive skin domains on the same mouse. Each domain cycles asynchronously — although hairs within each skin domain cycle in synchronized waves. Thus, the combinatorial defects in hair cycling and differentiation, together with concealed skin domains, account for the cyclic alopecia phenotype.
Key words: Alopecia, Hair cycle, Hair differentiation, Homeobox genes, Msx2, Foxn1, Ha3, Fgf5, Mouse
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