Mou Chunyan, Jackson Ben, Schneider Pascal, Overbeek Paul A, Headon Denis J
Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, United Kingdom.
Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9075-80. doi: 10.1073/pnas.0600825103. Epub 2006 Jun 12.
Hair follicles are spaced apart from one another at regular intervals through the skin. Although follicles are predominantly epidermal structures, classical tissue recombination experiments indicated that the underlying dermis defines their location during development. Although many molecules involved in hair follicle formation have been identified, the molecular interactions that determine the emergent property of pattern formation have remained elusive. We have used embryonic skin cultures to dissect signaling responses and patterning outcomes as the skin spatially organizes itself. We find that ectodysplasin receptor (Edar)-bone morphogenetic protein (BMP) signaling and transcriptional interactions are central to generation of the primary hair follicle pattern, with restriction of responsiveness, rather than localization of an inducing ligand, being the key driver in this process. The crux of this patterning mechanism is rapid Edar-positive feedback in the epidermis coupled with induction of dermal BMP4/7. The BMPs in turn repress epidermal Edar and hence follicle fate. Edar activation also induces connective tissue growth factor, an inhibitor of BMP signaling, allowing BMP action only at a distance from their site of synthesis. Consistent with this model, transgenic hyperactivation of Edar signaling leads to widespread overproduction of hair follicles. This Edar-BMP activation-inhibition mechanism appears to operate alongside a labile prepattern, suggesting that Edar-mediated stabilization of beta-catenin active foci is a key event in determining definitive follicle locations.
毛囊在皮肤中以规则的间隔彼此分开。尽管毛囊主要是表皮结构,但经典的组织重组实验表明,其下方的真皮在发育过程中决定了它们的位置。尽管已经鉴定出许多参与毛囊形成的分子,但决定模式形成这一新兴特性的分子相互作用仍然难以捉摸。我们利用胚胎皮肤培养来剖析信号反应和模式形成结果,因为皮肤会在空间上自行组织。我们发现,外胚层发育不良受体(Edar)-骨形态发生蛋白(BMP)信号传导和转录相互作用对于初级毛囊模式的形成至关重要,在此过程中,反应性的限制而非诱导配体的定位是关键驱动因素。这种模式形成机制的关键在于表皮中快速的Edar阳性反馈以及真皮BMP4/7的诱导。BMP反过来会抑制表皮Edar,从而抑制毛囊命运。Edar激活还会诱导结缔组织生长因子,这是一种BMP信号传导的抑制剂,使得BMP仅在远离其合成位点处发挥作用。与该模型一致,Edar信号的转基因过度激活会导致毛囊广泛过度生成。这种Edar-BMP激活-抑制机制似乎与一种不稳定的预模式一起发挥作用,这表明Edar介导的β-连环蛋白活性灶的稳定是决定最终毛囊位置的关键事件。