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.
`Cyclic alopecia' in Msx2 mutants: defects in hair cycling and hair shaft differentiation
Liang Ma, Jian Liu, Tobey Wu, Maksim Plikus, Ting-Xin Jiang, Qun Bi, Yi-Hsin Liu, Sven Müller-Röver, Heiko Peters, John P. Sundberg, Rob Maxson, Richard L. Maas, Cheng-Ming Chuong; `Cyclic alopecia' in Msx2 mutants: defects in hair cycling and hair shaft differentiation. Development 15 January 2003; 130 (2): 379–389. doi: https://doi.org/10.1242/dev.00201
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