Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Bioessays. 2024 Sep;46(9):e2400133. doi: 10.1002/bies.202400133. Epub 2024 Jul 11.
The vertebrate retina is a tractable system for studying control of cell neurogenesis and cell fate specification. During embryonic development, retinal neurogenesis is under strict temporal regulation, with cell types generated in fixed but overlapping temporal intervals. The temporal sequence and relative numbers of retinal cell types generated during development are robust and show minimal experience-dependent variation. In many cold-blooded vertebrates, acute retinal injury induces a different form of neurogenesis, where Müller glia reprogram into retinal progenitor-like cells that selectively regenerate retinal neurons lost to injury. The extent to which the molecular mechanisms controlling developmental and injury-induced neurogenesis resemble one another has long been unclear. However, a recent study in zebrafish has shed new light on this question, using single-cell multiomic analysis to show that selective loss of different retinal cell types induces the formation of fate-restricted Müller glia-derived progenitors that differ both from one another and from progenitors in developing retina. Here, we discuss the broader implications of these findings, and their possible therapeutic relevance.
脊椎动物的视网膜是研究细胞神经发生和细胞命运特化控制的一个易于处理的系统。在胚胎发育过程中,视网膜神经发生受到严格的时间调控,细胞类型在固定但重叠的时间间隔内产生。在发育过程中产生的视网膜细胞类型的时间顺序和相对数量是稳健的,表现出最小的经验依赖性变化。在许多冷血脊椎动物中,急性视网膜损伤会诱导一种不同形式的神经发生,其中 Müller 胶质细胞重新编程为类似于视网膜祖细胞的细胞,这些细胞选择性地再生因损伤而丧失的视网膜神经元。控制发育和损伤诱导神经发生的分子机制在多大程度上相似,长期以来一直不清楚。然而,最近在斑马鱼中的一项研究通过单细胞多组学分析揭示了这个问题,该研究表明,不同的视网膜细胞类型的选择性缺失会诱导形成命运受限的 Müller 胶质细胞衍生的祖细胞,这些祖细胞彼此不同,也与发育中的视网膜祖细胞不同。在这里,我们讨论了这些发现的更广泛意义及其可能的治疗相关性。