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Inherited apicobasal polarity defines the key features of axon-dendrite polarity in a sensory neuron
Current Biology ( IF 9.2 ) Pub Date : 2021-07-15 , DOI: 10.1016/j.cub.2021.06.039
Joo Lee 1 , Jérémy Magescas 1 , Richard D Fetter 2 , Jessica L Feldman 1 , Kang Shen 2
Affiliation  

Neurons are highly polarized cells with morphologically and functionally distinct dendritic and axonal processes. The molecular mechanisms that establish axon-dendrite polarity in vivo are poorly understood. Here, we describe the initial polarization of posterior deirid (PDE), a ciliated mechanosensory neuron, during development in vivo through 4D live imaging with endogenously tagged proteins. PDE inherits and maintains apicobasal polarity from its epithelial precursor. Its apical domain is directly transformed into the ciliated dendritic tip through apical constriction, which is followed by axonal outgrowth from the opposite basal side of the cell. The apical Par complex and junctional proteins persistently localize at the developing dendritic domain throughout this transition. Consistent with their instructive role in axon-dendrite polarization, conditional depletion of the Par complex and junctional proteins results in robust defects in dendrite and axon formation. During apical constriction, a microtubule-organizing center (MTOC) containing the microtubule nucleator γ-tubulin ring complex (γ-TuRC) forms along the apical junction between PDE and its sister cell in a manner dependent on the Par complex and junctional proteins. This junctional MTOC patterns neuronal microtubule polarity and facilitate the dynein-dependent recruitment of the basal body for ciliogenesis. When non-ciliated neurons are genetically manipulated to obtain ciliated neuronal fate, inherited apicobasal polarity is required for generating ciliated dendritic tips. We propose that inherited apicobasal polarity, together with apical cell-cell interactions drive the morphological and cytoskeletal polarity in early neuronal differentiation.



中文翻译:

遗传的顶基极性定义了感觉神经元中轴突-树突极性的关键特征

神经元是高度极化的细胞,具有形态和功能上不同的树突和轴突过程。在体内建立轴突-树突极性的分子机制知之甚少。在这里,我们描述了后 deirid (PDE) 的初始极化,一种纤毛机械感觉神经元,在体内发育过程中通过内源性标记蛋白质的 4D 实时成像。PDE 继承并维持其上皮前体的 apicobasal 极性。其顶端结构域通过顶端收缩直接转化为纤毛树突尖端,随后轴突从细胞的相对基底侧生长。在整个转变过程中,顶端 Par 复合物和连接蛋白持续定位于发育中的树突结构域。与它们在轴突-树突极化中的指导作用一致,Par 复合物和连接蛋白的条件消耗导致树突和轴突形成的严重缺陷。在根尖收缩期间,含有微管成核剂γ-微管蛋白环复合物(γ-TuRC)的微管组织中心(MTOC)以依赖于Par复合物和连接蛋白的方式沿着PDE与其姐妹细胞之间的顶端连接处形成。这种连接的 MTOC 模式神经元微管极性并促进纤毛发生的基体的动力蛋白依赖性募集。当对非纤毛神经元进行基因操作以获得纤毛神经元命运时,需要遗传的顶基极性来产生纤毛树突尖端。我们提出遗传的顶基极性,连同顶端细胞-细胞相互作用驱动早期神经元分化中的形态和细胞骨架极性。这种连接的 MTOC 模式神经元微管极性并促进纤毛发生的基体的动力蛋白依赖性募集。当对非纤毛神经元进行基因操作以获得纤毛神经元命运时,需要遗传的顶基极性来产生纤毛树突尖端。我们提出遗传的顶基极性,连同顶端细胞-细胞相互作用驱动早期神经元分化中的形态和细胞骨架极性。这种连接的 MTOC 模式神经元微管极性并促进纤毛发生的基体的动力蛋白依赖性募集。当对非纤毛神经元进行基因操作以获得纤毛神经元命运时,需要遗传的顶基极性来产生纤毛树突尖端。我们提出遗传的顶基极性,连同顶端细胞-细胞相互作用驱动早期神经元分化中的形态和细胞骨架极性。

更新日期:2021-09-13
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