MSX GENES AND HAIR DEVELOPMENT

哺乳动物的毛囊是由一系列复杂的相互作用而形成的 在表皮和真皮之间 一个基因家族 在这一过程中潜在重要的是Msx同源框基因， 已经证明在介导上皮-间质细胞 哺乳动物器官发生过程中的相互作用。 Msx 2缺陷小鼠 有牙齿、胃、乳腺、生长板，最明显的是， 毛发和皮肤表型。 msx 2基因敲除小鼠出生并表现正常 与出生后第15天的同窝仔相比， 从头到尾逐渐谢顶 观察到几个缺陷 Msx 2突变体的皮肤和毛发 Msx 2基因敲除小鼠的皮毛 如果用蛋白质流质食物喂养， 10天后再次脱毛。 我们检测了这两种基因的表达模式， Msx 1和Msx 2在第一个头发周期使用原位杂交。 Msx 1和Msx 2都在P8前的萌发基质中表达。 此后，Msx 2的表达结构域扩展到包括内部的 Msx 1的外根鞘可能也有变化。 到P17，在毛囊中没有检测到Msx 1表达， Msx 2表达持续存在。 时间和空间的差异 Msx 1和Msx 2的表达式可以解释为什么Msx 1不能补偿 毛囊中Msx 2突变的基因 功能冗余 在器官发生过程中Msx 1和Msx 2之间的联系进一步得到了 Msx 1和Msx 2缺陷小鼠的产生， 身体的许多器官都受到了影响。 毛囊发育 在双突变胚胎中， 相比之下，只有三分之一的卵泡被诱导 野生型胚胎 表皮标志物Sonic Hedgehog的表达 (shh)双突变皮肤中的皮肤标记Patched（ptc）出现 然而，与野生型相比， 场地减少了。 我们认为Msx基因在 无论是早期的毛囊诱导过程，并在以后的头发生长周期。

Mammalian hair follicles develop from a series of complex interactions between the epidermis and the underlying dermis. One family of genes potentially important in this process is the Msx homeobox genes which have been shown to be important in mediating epithelial-mesenchymal interactions during mammalian organogenesis. Msx2-deficient mice exhibit tooth, stomach, mammary gland, growth plate and most noticeably, hair and skin phenotypes. Msx2 null mice are born and appear normal compared to their littermates until postnatal day 15, then exhibit progressive balding from head to tail. Several defects were observed in Msx2 mutant skin and hair. The pelage hair on Msx2 null mice will grown back if they are fed with a proteinous liquid diet, only to epilate again in 10 days. We examined the expression pattern of both Msx1 and Msx2 during the first hair cycle using in situ hybridization. Both Msx1 and Msx2 are expressed in the germinative matrix before P8. Thereafter, the expression domain of Msx2 expands to include the inner and possibly the outer root sheath while that of Msx1 remains unchanged. By P17, no Msx1 expression in the hair follicle can be detected whereas Msx2 expression persists. The differences in temporal and spatial expression of Msx1 and Msx2 might explain why Msx1 fails to compensate for the Msx2 mutation in the hair follicle. Functional redundancy between Msx1 and Msx2 during organogenesis is further supported by the generation of mice deficient for both Msx1 and Msx2 in which development of numerous organs in the body is affected. Hair follicle development in double mutant embryos is affected at the follicle induction stage in which only one third the number of follicles are induced compared to wild-type embryos. Expression of the epidermal marker Sonic Hedgehog (shh) and dermal marker Patched (ptc) in double mutant skin appears comparable to wild type, however, the number of shh and ptc expression sites is reduced. We propose that Msx genes play important roles in both early follicle induction process and in later hair growth cycles.