'Cyclic alopecia' in Msx2 mutants:: defects in hair cycling and hair shaft differentiation

被引:124
|
作者
Ma, L
Liu, J
Wu, T
Plikus, M
Jiang, TX
Bi, Q
Liu, YH
Müller-Röver, S
Peters, H
Sundberg, JP
Maxson, R
Maas, RL [1 ]
Chuong, CM
机构
[1] Univ So Calif, Dept Pathol, Los Angeles, CA 90033 USA
[2] Brigham & Womens Hosp, Dept Med, Div Genet, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Boston, MA 02115 USA
[4] Tulane Univ, Dept Cell & Mol Biol, New Orleans, LA 70118 USA
[5] Univ So Calif, Ctr Craniofacial Mol Biol, Los Angeles, CA 90033 USA
[6] Univ Hamburg, Hosp Eppendorf, Dept Dermatol, D-20246 Hamburg, Germany
[7] Jackson Lab, Bar Harbor, ME 04069 USA
[8] Univ So Calif, Dept Biochem, Los Angeles, CA 90033 USA
来源
DEVELOPMENT | 2003年 / 130卷 / 02期
关键词
alopecia; hair cycle; hair differentiation; homeobox genes; Msx2; Foxn1; Ha3; Fgf5; mouse;
D O I
10.1242/dev.00201
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:379 / 389
页数:11
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