PDF(Pubmed)
Abstract：
Lgl1 protein plays a critical role in neurodevelopment, including hippocampus, olfactory bulb, and Purkinje cell. However, the specific mechanism of LGL1 function in the midbrain remains elusive. In this study, we generated Lgl1 conditional knockout mice using Pax2-Cre, which is expressed in the midbrain, and examined the functions of Lgl1 in the midbrain. Histological analysis exhibited abnormal midbrain development characterized by enlarged ventricular aqueduct and thinning tectum cortex. Lgl1 deletion caused excessive proliferation and heightened apoptosis of neural progenitor cells in the tectum of LP cko mice. BrdU labeling studies demonstrated abnormal neuronal migration. Immunofluorescence analysis of Nestin demonstrated an irregular and clustered distribution of glial cell fibers, with the adhesion junction marker N-cadherin employed for immunofluorescent labeling, unveiling abnormal epithelial connections within the tectum of LP cko mice. The current findings suggest that the deletion of Lgl1 leads to the disruption of the expression pattern of N-cadherin, resulting in abnormal development of the midbrain.
摘要：
Lgl1蛋白在神经发育中起关键作用，包括海马,嗅觉灯泡,和浦肯野细胞。然而,中脑LGL1功能的具体机制仍然难以捉摸。在这项研究中,我们使用Pax2-Cre产生了Lgl1条件性敲除小鼠，在中脑表达，并检查了Lgl1在中脑的功能。组织学分析显示中脑发育异常，其特征是心室导水管增大和顶盖皮质变薄。Lgl1缺失导致LPcko小鼠顶盖中神经祖细胞的过度增殖和凋亡增加。BrdU标记研究表明神经元迁移异常。Nestin的免疫荧光分析显示神经胶质细胞纤维的不规则和聚集分布，使用用于免疫荧光标记的粘附连接标记N-cadherin，揭示LPcko小鼠顶盖内异常的上皮连接。目前的研究结果表明，Lgl1的缺失导致N-cadherin表达模式的破坏，导致中脑发育异常.
