PDF(Pubmed)
Abstract：
The retina has diverse neuronal cell types derived from a common pool of retinal progenitors. Many molecular drivers, mostly transcription factors, have been identified to promote different cell fates. In Drosophila, atonal is required for specifying photoreceptors. In mice, there are two closely related atonal homologs, Atoh1 and Atoh7 While Atoh7 is known to promote the genesis of retinal ganglion cells, there is no study on the function of Atoh1 in retinal development. Here, we crossed Atoh1Cre/+ mice to mice carrying a Cre-dependent TdTomato reporter to track potential Atoh1-lineage neurons in retinas. We characterized a heterogeneous group of TdTomato+ retinal neurons that were detected at the postnatal stage, including glutamatergic amacrine cells, AII amacrine cells, and BC3b bipolar cells. Unexpectedly, we did not observe TdTomato+ retinal neurons in the mice with an Atoh1-FlpO knock-in allele and a Flp-dependent TdTomato reporter, suggesting Atoh1 is not expressed in the mouse retina. Consistent with these data, conditional removal of Atoh1 in the retina did not cause any observable phenotypes. Importantly, we did not detect Atoh1 expression in the retina at multiple ages using mice with Atoh1-GFP knock-in allele. Therefore, we conclude that Atoh1Cre/+ mice have ectopic Cre expression in the retina and that Atoh1 is not required for retinal development.
摘要：
视网膜具有源自共同的视网膜祖细胞池的多种神经元细胞类型。许多分子驱动因素，主要是转录因子，已被确定为促进不同的细胞命运。在果蝇中,指定光感受器需要无调。在老鼠身上,有两个密切相关的无调性同源物，Atoh1和Atoh7虽然已知Atoh7促进视网膜神经节细胞的发生，目前尚无Atoh1在视网膜发育中的功能研究。这里,我们将Atoh1Cre/+小鼠与携带Cre依赖性TdTomato报告基因的小鼠交叉，以追踪视网膜中潜在的Atoh1谱系神经元。我们表征了在出生后阶段检测到的一组异质的TdTomato+视网膜神经元，包括谷氨酸能无长突细胞，AII无长突细胞，和BC3b双极细胞。出乎意料的是,我们没有在具有Atoh1-FlpO敲入等位基因和Flp依赖性TdTomato报告基因的小鼠中观察到TdTomato+视网膜神经元，提示Atoh1在小鼠视网膜中不表达。与这些数据一致，有条件去除视网膜中的Atoh1不会导致任何可观察到的表型。重要的是,我们使用具有Atoh1-GFP基因敲入等位基因的小鼠,在多个年龄未检测到视网膜中Atoh1的表达.因此,我们得出的结论是，Atoh1Cre/小鼠在视网膜中有异位Cre表达，并且Atoh1不是视网膜发育所必需的。
