科学家可能发现了导致小鼠的毛发周期性脱落的遗传机制，而且提出同样的原因可能造成的人类毛发脱落，即脱发症。通常，毛发经历了一个生长、静止和脱落的过程，之后生长重新开始。

Yumiko Saga和同事报告说，缺乏Sox21基因的小鼠表现出了从头到尾的进行性的毛发脱落、几天后毛发重新生长的循环。这组作者发现，Sox21帮助调控了角蛋白——毛发的蛋白质基本成分——的合成，而且证明了没有这个基因的小鼠与Sox21基因水平正常的小鼠相比，前者的毛发构建蛋白减少。这种遗传改造小鼠还在毛囊周围有增大的分泌油的皮脂腺，而且在毛发脱落期的皮肤细胞层变厚。这组作者提出，这个基因很可能参与了形成毛干的外层的干细胞的分化。对人类皮肤样本的检查证实了在毛发外层Sox21基因的高度表达。这组作者得出结论说，这些结果表明Sox21基因可能导致了人类的一些毛发脱落病症。

推荐原始出处：

PNAS May 26, 2009, doi: 10.1073/pnas.0808324106

The disruption of Sox21-mediated hair shaft cuticle differentiation causes cyclic alopecia in mice

Makoto Kisoa,1, Shigekazu Tanakab,1, Rie Sabaa, Satoru Matsudac, Atsushi Shimizud, Manabu Ohyamad, Hirotaka James Okanoc, Toshihiko Shiroishib,e, Hideyuki Okanoc and Yumiko Sagaa,e,2

Hair is maintained through a cyclic process that includes periodic regeneration of hair follicles in a stem cell-dependent manner. Little is known, however, about the cellular and molecular mechanisms that regulate the layered differentiation of the hair follicle. We have established a mutant mouse with a cyclic alopecia phenotype resulting from the targeted disruption of Sox21, a gene that encodes a HMG-box protein. These mice exhibit progressive hair loss after morphogenesis of the first hair follicle and become completely nude in appearance, but then show hair regrowth. Sox21 is expressed in the cuticle layer and the progenitor cells of the hair shaft in both mouse and human. The lack of this gene results in a loss of the interlocking structures required for anchoring the hair shaft in the hair follicle. Furthermore, the expression of genes encoding the keratins and keratin binding proteins in the hair shaft cuticle are also specifically down-regulated in the Sox21-null mouse. These results indicate that Sox21 is a master regulator of hair shaft cuticle differentiation and shed light on the possible causes of human hair disorders.