Rodriguez Viales Rebecca, Diotel Nicolas, Ferg Marco, Armant Olivier, Eich Julia, Alunni Alessandro, März Martin, Bally-Cuif Laure, Rastegar Sepand, Strähle Uwe
Karlsruhe Institute of Technology, Institute of Toxicology and Genetics, Karlsruhe, Germany.
Stem Cells. 2015 Mar;33(3):892-903. doi: 10.1002/stem.1883.
The teleost brain has the remarkable ability to generate new neurons and to repair injuries during adult life stages. Maintaining life-long neurogenesis requires careful management of neural stem cell pools. In a genome-wide expression screen for transcription regulators, the id1 gene, encoding a negative regulator of E-proteins, was found to be upregulated in response to injury. id1 expression was mapped to quiescent type I neural stem cells in the adult telencephalic stem cell niche. Gain and loss of id1 function in vivo demonstrated that Id1 promotes stem cell quiescence. The increased id1 expression observed in neural stem cells in response to injury appeared independent of inflammatory signals, suggesting multiple antagonistic pathways in the regulation of reactive neurogenesis. Together, we propose that Id1 acts to maintain the neural stem cell pool by counteracting neurogenesis-promoting signals.
硬骨鱼的大脑在成年生命阶段具有生成新神经元和修复损伤的非凡能力。维持终身神经发生需要对神经干细胞库进行精细管理。在一项针对转录调节因子的全基因组表达筛选中，发现编码E蛋白负调节因子的id1基因在损伤反应中上调。id1表达定位于成年端脑干细胞生态位中的静止I型神经干细胞。体内id1功能的获得和丧失表明Id1促进干细胞静止。在神经干细胞中观察到的对损伤反应中id1表达的增加似乎独立于炎症信号，这表明在反应性神经发生的调节中有多种拮抗途径。我们共同提出，Id1通过抵消促进神经发生的信号来维持神经干细胞库。
