Brinkmann Bastian G, Quintes Susanne
Max Planck Institute of Experimental Medicine, Department of Neurogenetics , Göttingen, Germany.
Max Planck Institute of Experimental Medicine, Department of Neurogenetics, Göttingen, Germany; University Medical Center Göttingen (UMG), Department of Clinical Neurophysiology, Göttingen, Germany.
Neurogenesis (Austin). 2017 Feb 2;4(1):e1271495. doi: 10.1080/23262133.2016.1271495. eCollection 2017.
Development of Schwann cells is tightly regulated by concerted action of activating and inhibiting factors. Most of the regulatory feedback loops identified to date are transcriptional activators promoting induction of genes coding for integral myelin proteins and lipids. The mechanisms by which inhibitory factors are silenced during Schwann cell maturation are less well understood. We could recently show a pivotal function for the transcription factor zinc finger E-box binding homeobox 2 (Zeb2) during Schwann cell development and myelination as a transcriptional repressor of maturation inhibitors. Zeb2 belongs to a family of highly conserved 2-handed zinc-finger proteins and represses gene transcription by binding to E-box sequences in the regulatory region of target genes. The protein is known to repress E-cadherin during epithelial to mesenchymal transition (EMT) in tumor malignancy and mediates its functions by interacting with multiple co-factors. During nervous system development, Zeb2 is expressed in neural crest cells, the precursors of Schwann cells, the myelinating glial cells of peripheral nerves. Schwann cells lacking Zeb2 fail to fully differentiate and are unable to sort and myelinate peripheral nerve axons. The maturation inhibitors Sox2, Ednrb and Hey2 emerge as targets for Zeb2-mediated transcriptional repression and show persistent aberrant expression in Zeb2-deficient Schwann cells. While dispensible for adult Schwann cells, re-activation of Zeb2 is essential after nerve injury to allow remyelination and functional recovery. In summary, Zeb2 emerges as an "inhibitor of inhibitors," a novel concept in Schwann cell development and nerve repair.
施万细胞的发育受到激活因子和抑制因子协同作用的严格调控。迄今为止确定的大多数调节反馈回路都是转录激活因子,促进编码整合髓磷脂蛋白和脂质的基因的诱导。在施万细胞成熟过程中抑制因子被沉默的机制尚不太清楚。我们最近发现转录因子锌指E盒结合同源框2(Zeb2)在施万细胞发育和髓鞘形成过程中作为成熟抑制剂的转录抑制因子发挥关键作用。Zeb2属于一类高度保守的双手锌指蛋白家族,通过与靶基因调控区域的E盒序列结合来抑制基因转录。已知该蛋白在肿瘤恶性上皮-间质转化(EMT)过程中抑制E-钙黏蛋白,并通过与多种辅助因子相互作用来介导其功能。在神经系统发育过程中,Zeb2在神经嵴细胞中表达,神经嵴细胞是施万细胞的前体,也是周围神经的髓鞘形成胶质细胞。缺乏Zeb2的施万细胞无法完全分化,并且无法对周围神经轴突进行分类和髓鞘化。成熟抑制剂Sox2、Ednrb和Hey2成为Zeb2介导的转录抑制的靶点,并在缺乏Zeb2的施万细胞中持续异常表达。虽然Zeb2对成年施万细胞并非必需,但在神经损伤后重新激活Zeb2对于实现髓鞘再生和功能恢复至关重要。总之,Zeb2成为一种“抑制剂的抑制剂”,这是施万细胞发育和神经修复中的一个新概念。