Misexpression of cNSCL1 disrupts retinal development
Misexpression of cNSCL1 disrupts retinal development
复制标题
DOI：
10.1006/mcne.1999.0765
复制
发表时间：
1999-07-01
影响因子：
3.5
通讯作者：
Wang, SZ
中科院分区：
文献类型：
--
作者：
Li, CM;Yan, RT;Wang, SZ
cNSCL 1是哺乳动物NSCL 1的鸡同源物，NSCL 1是在神经发生期间瞬时表达的碱性螺旋-环-螺旋基因。为了深入了解其功能，我们研究了cNSCL 1在视网膜神经发生中的参与。原位杂交显示cNSCL 1的动态，细胞类型特异性表达，首先在发展中的神经节细胞，后来在神经胶质细胞。这与neuroD在年轻感光细胞及其前体中的表达截然不同，表明所提出的neurogenin --> neuroD --> NSCL 1级联可能不适用于小鸡的视网膜神经发生。当cNSCL 1通过病毒转导在视网膜神经上皮中错误表达时，产生小眼睛。用BrdU和[（3）H]胸苷脉冲标记显示cNSCL 1错误表达的细胞增殖活性显著降低。大量的细胞死亡发生，但只有在细胞增殖活动已经消退，导致视网膜结构的主要扭曲。我们的数据表明，在视网膜发育过程中调控cNSCL 1表达的重要性。
cNSCL1 is the chick homologue of mammalian NSCL1, a basic helix-loop-helix gene transiently expressed during neurogenesis. To gain insight into its function, we studied the involvement of cNSCL1 in retinal neurogenesis. In situ hybridization showed dynamic, cell-type-specific expression of cNSCL1, first in developing ganglion cells and later in glial cells. This is drastically different from the expression of neuroD in young photoreceptor cells and their precursors, demonstrating that the proposed neurogenin --> neuroD --> NSCL1 cascade might not apply to retinal neurogenesis in the chick. Small eyes were produced when cNSCL1 was misexpressed in the retinal neuroepithelium through viral transduction. Pulse-labeling with BrdU and [(3)H]thymidine revealed a significant decrease in cell proliferation activity with cNSCL1 misexpression. Massive cell death occurred, but only after cell proliferation activity had subsided, resulting in major distortions of retinal structure. Our data demonstrate the importance of regulated expression of cNSCL1 during retinal development.