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Abstract：
In the vertebrate retina six types of neurons and one glial cell type are generated from multipotent retinal progenitor cells (RPCs) whose proliferation and differentiation are regulated by intrinsic and extrinsic factors. RPCs proliferate undergoing interkinetic nuclear migration within the neuroblastic layer, with their nuclei moving up and down along the apico-basal axis. Moreover, they only differentiate and therefore exit the cell cycle at the apical side of the neuroblastic layer. Sema6A and its receptors PlexinA4 and PlexinA2 control lamina stratification of the inner plexiform layer in the mouse retina. Nevertheless, their function in earlier developmental stages is still unknown. Here, we analyzed the embryonic retina of PlexinA2 and Sema6A knockout mice. Using time-lapse videomicroscopy we provide evidence that Sema6A/PlexinA2 signaling participates to interkinetic nuclear migration of RPCs around birth. When disrupted, RPCs migration is blocked at the apical side of the neuroblastic layer. This is the first evidence supporting a role for transmembrane molecules in the regulation of interkinetic nuclear migration in the mouse retina.
摘要：
在脊椎动物视网膜中，多能视网膜祖细胞（RPC）产生了六种类型的神经元和一种神经胶质细胞类型，其增殖和分化受内在和外在因素的调节。RPCs在神经母细胞层内经历动力间核迁移而增殖，它们的细胞核沿着根尖轴上下移动。此外，它们仅在神经母细胞层的顶端分化并因此退出细胞周期。Sema6A及其受体PlexinA4和PlexinA2控制小鼠视网膜内网状层的层分层。然而，它们在早期发育阶段的功能仍然未知。这里,我们分析了PlexinA2和Sema6A基因敲除小鼠的胚胎视网膜。使用延时视频显微镜，我们提供了证据，证明Sema6A/PlexinA2信号参与了出生前后RPC的动力间核迁移。当中断时，RPCs的迁移在神经母细胞层的顶端被阻断。这是第一个证据，支持跨膜分子在调节小鼠视网膜运动间核迁移中的作用。
