Pou4f2-GFP knock-in mouse line: A model for studying retinal ganglion cell development
Pou4f2-GFP knock-in mouse line: A model for studying retinal ganglion cell development
复制标题
Pou4f2-GFP 敲入小鼠系：研究视网膜神经节细胞发育的模型
作者：
王宇英
Pou 4f 2在全面的、逐步的基因调控网络（GRN）中起关键节点的作用，并调控视网膜神经节细胞（RGC）的发育。因此，Pou 4f 2的缺失导致RGC轴突缺陷和凋亡。为了研究参与RGC再生的GRN，我们产生了具有在RGC中表达的POU 4F 2-绿色荧光蛋白（GFP）融合蛋白的小鼠系。使用免疫荧光分析证实POU 4F 2和GFP在Pou 4f 2-GFP/+杂合子小鼠的视网膜和脑中的共定位。与野生型小鼠相比，Pou 4f 2-GFP/GFP纯合子小鼠POU 4F 2和POU 4F 1的表达模式以及ISL 1和POU 4F 2的共表达模式未受影响。此外，RGC的定量显示Pou 4f 2-GFP/GFP纯合子和野生型小鼠之间没有显著差异。这些结果表明，Pou 4f 2-GFP/GFP纯合子小鼠的RGCs发育与野生型小鼠相同。因此，本Pou 4f 2-GFP敲入小鼠系是进一步研究RGCs分化和再生的有用工具。
Pou4f2acts as a key node in the comprehensive and step‐wise gene regulatory network (GRN) and regulates the development of retinal ganglion cells (RGCs). Accordingly, deletion ofPou4f2results in RGC axon defects and apoptosis. To investigate the GRN involved in RGC regeneration, we generated a mouse line with a POU4F2‐green fluorescent protein (GFP) fusion protein expressed in RGCs. Co‐localization of POU4F2 and GFP in the retina and brain ofPou4f2‐GFP/+heterozygote mice was confirmed using immunofluorescence analysis. Compared with those in wild‐type mice, the expression patterns of POU4F2 and POU4F1 and the co‐expression patterns of ISL1 and POU4F2 were unaffected inPou4f2‐GFP/GFPhomozygote mice. Moreover, the quantification of RGCs showed no significant difference betweenPou4f2‐GFP/GFPhomozygote and wild‐type mice. These results demonstrated that the development of RGCs inPou4f2‐GFP/GFPhomozygote mice was the same as in wild‐type mice. Thus, the presentPou4f2‐GFPknock‐in mouse line is a useful tool for further studies on the differentiation and regeneration of RGCs.