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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Control of late off-center cone bipolar cell differentiation and visual signaling by the homeobox gene Vsx1
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Control of late off-center cone bipolar cell differentiation and visual signaling by the homeobox gene Vsx1

机译：同源盒基因Vsx1控制晚期偏心圆锥双极细胞分化和视觉信号

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摘要

Retinal bipolar cells are interneurons that transmit visual signals from photoreceptors to ganglion cells. Although the visual pathways mediated by bipolar cells have been well characterized, the genes that regulate their development and function are largely unknown. To determine the role in bipolar cell development of the homeobox gene Vsx1, whose retinal expression is restricted to a major subset of differentiating and mature cone bipolar (CB) cells, we targeted the gene in mice. Bipolar cell fate was not altered in the absence of Vsx1 function, because the pan-bipolar markers Chx10 and Ret-B1 continued to be expressed in inner nuclear layer neurons labeled by the Vsx1-targeting reporter gene, τLacZ. The specification, number, and gross morphology of the subset of on-center and off-center (OFF)-CB cells defined by τLacZ expression from the Vsx1 locus were also normal in Vsx1~(τLacZ)/Vsx1~(τLacZ) mice. However, the terminal differentiation of OFF-CB cells in the retina of Vsx1~(τLacZ)/Vsx1~(τLacZ) mice was incomplete, as demonstrated by a substantial reduction in the expression of at least four markers (recoverin, NK3R, Neto1, and CaB5) for these interneurons. These molecular abnormalities were associated with defects in retinal function and documented by electroretinography and in vitro ganglion cell recordings specific to cone visual signaling. In particular, there was a general reduction in the light-mediated activity of OFF, but not on-center, ganglion cells. Thus, Vsx1 is required for the late differentiation and function of OFF-CB cells and is associated with a heritable OFF visual pathway-specific retinal defect.
机译：视网膜双极细胞是将神经信号从感光器传递到神经节细胞的中间神经元。尽管已经很好地表征了由双极细胞介导的视觉途径，但是调节其发育和功能的基因在很大程度上尚不清楚。为了确定同源盒基因Vsx1在双极细胞发育中的作用，该基因的视网膜表达仅限于分化和成熟的圆锥双极（CB）细胞的主要子集，我们将该基因定位于小鼠。在没有Vsx1功能的情况下，双极细胞的命运没有改变，因为泛双极标记Chx10和Ret-B1继续在靶向Vsx1的报告基因τLacZ标记的内核层神经元中表达。在Vsx1〜（τLacZ）/ Vsx1〜（τLacZ）小鼠中，由Vsx1基因座中的τLacZ表达定义的中心和偏心（OFF）-CB细胞子集的规格，数量和总体形态也正常。但是，Vsx1〜（τLacZ）/ Vsx1〜（τLacZ）小鼠视网膜中OFF-CB细胞的终末分化是不完全的，这至少可以通过至少四种标记物（recoverin，NK3R，Neto1，和CaB5）用于这些中间神经元。这些分子异常与视网膜功能缺陷有关，并通过视网膜电图和特定于视锥视觉信号的体外神经节细胞记录来证明。特别是，OFF的光介导活性普遍下降，但中心神经节细胞却没有下降。因此，Vsx1是OFF-CB细胞的后期分化和功能所必需的，并且与遗传性OFF视觉通路特异性视网膜缺损有关。

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