Retinal ganglion cells (RGCs), which relay visual information from the eye to the brain, are the first cell type generated during retinal neurogenesis. Loss of function of the transcription factor Atoh7, which is expressed in multipotent early neurogenic retinal progenitor cells, leads to a selective and near complete loss of RGCs. Atoh7 has thus been considered essential for conferring competence on progenitors to generate RGCs. However, when apoptosis is inhibited in Atoh7-deficient mice by loss of function of Bax, only a modest reduction in RGC number is observed. Single-cell RNA-Seq of Atoh7;Bax-deficient retinas shows that RGC differentiation is delayed, but that RGC precursors are grossly normal. Atoh7;Bax-deficient RGCs eventually mature, fire action potentials, and incorporate into retinal circuitry, but exhibit severe axonal guidance defects. This study reveals an essential role for Atoh7 in RGC survival, and demonstrates Atoh7-independent mechanisms for RGC specification.

中文翻译：

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视网膜神经节细胞身份的Atoh7独立规格

视网膜神经节细胞（RGCs）将视觉信息从眼睛传递到大脑，是视网膜神经发生过程中产生的第一类细胞。在多能性早期神经源性视网膜祖细胞中表达的转录因子Atoh7的功能丧失导致RGC的选择性丧失和接近完全丧失。因此，Atoh7被认为对赋予祖细胞产生RGC的能力至关重要。但是，当通过Bax功能丧失在Atoh7缺陷型小鼠中抑制凋亡时，仅观察到RGC数量的适度降低。Atoh7；缺乏Bax的视网膜的单细胞RNA-Seq显示RGC分化被延迟，但是RGC前体基本上是正常的。Atoh7;缺乏Bax的RGC最终会成熟，具有发火作用，并整合到视网膜电路中，但表现出严重的轴突引导缺陷。这项研究揭示了Atoh7在RGC生存中的重要作用，并证明了RGC规范的Atoh7独立机制。