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蛋白O-连接岩藻糖基转移酶1(Pofut1)基因缺失可导致Notch分子无法与配体结合并启动信号传递.为研究Pofut1基因对哺乳动物胚胎干细胞(ESC)向神经分化的影响,利用Pofut1基因敲除的胚胎干细胞与野生型胚胎干细胞,经体外培养诱导拟胚体(EB)分化为神经细胞,计数分化为神经细胞的比例,采用细胞免疫组化染色和real-time PCR等方法,分析神经细胞特异性标志分子的表达.结果显示,Pofut1基因缺失后,对EBC生长没有明显影响,分化过程中形成的拟胚体数量明显增多,分化的神经样细胞以及神经标志物分子的表达也明显多于对照组;Notch信号缺失对小鼠胚胎干细胞生长无明显影响,但可以促进ES细胞向神经细胞分化.
Deletion of the O-linked Pofut1 gene leads to the inability of Notch to bind to the ligand and initiates signaling.In order to study the effect of Pofut1 on the neural differentiation of mammalian embryonic stem cells (ESC), Pofut1 Gene knockout embryonic stem cells and wild-type embryonic stem cells were induced to differentiate into neural cells by counting the number of differentiated neural cells in vitro. Immunocytochemical staining and real-time PCR were used to analyze the expression of EBs. The results showed that the deletion of Pofut1 gene had no significant effect on the growth of EBC, the number of embryoid bodies formed during differentiation significantly increased, and the expression of differentiated neuron-like cells and neuronal markers was also significant More than the control group; Notch signal deletion had no significant effect on the growth of mouse embryonic stem cells, but could promote the differentiation of ES cells into neurons.