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激素控制有丝后神经元分化状态的变化。

Hormone-controlled changes in the differentiation state of post-mitotic neurons.

机构信息

Institute of Cellular and Organismic Biology, Academia Sinica, Academia Road, Taipei 11529, Taiwan; Institute of Molecular and Cellular Biology, College of Life Science, National Taiwan University, Roosevelt Road, Taipei 10617, Taiwan.

Howard Hughes Medical Institute, Janelia Research Campus, Helix Drive, Ashburn, VA 20147, USA.

出版信息

Curr Biol. 2022 May 23;32(10):2341-2348.e3. doi: 10.1016/j.cub.2022.04.027. Epub 2022 May 3.

DOI:10.1016/j.cub.2022.04.027
PMID:35508173
Abstract

While we think of neurons as having a fixed identity, many show spectacular plasticity. Metamorphosis drives massive changes in the fly brain; neurons that persist into adulthood often change in response to the steroid hormone ecdysone. Besides driving remodeling, ecdysone signaling can also alter the differentiation status of neurons. The three sequentially born subtypes of mushroom body (MB) Kenyon cells (γ, followed by α'/β', and finally α/β) serve as a model of temporal fating. γ neurons are also used as a model of remodeling during metamorphosis. As γ neurons are the only functional Kenyon cells in the larval brain, they serve the function of all three adult subtypes. Correspondingly, larval γ neurons have a similar morphology to α'/β' and α/β neurons-their axons project dorsally and medially. During metamorphosis, γ neurons remodel to form a single medial projection. Both temporal fate changes and defects in remodeling therefore alter γ-neuron morphology in similar ways. Mamo, a broad-complex, tramtrack, and bric-à-brac/poxvirus and zinc finger (BTB/POZ) transcription factor critical for temporal specification of α'/β' neurons, was recently described as essential for γ remodeling. In a previous study, we noticed a change in the number of adult Kenyon cells expressing γ-specific markers when mamo was manipulated. These data implied a role for Mamo in γ-neuron fate specification, yet mamo is not expressed in γ neurons until pupariation, well past γ specification. This indicates that mamo has a later role in ensuring that γ neurons express the correct Kenyon cell subtype-specific genes in the adult brain.

摘要

虽然我们认为神经元具有固定的身份,但许多神经元表现出惊人的可塑性。变态会导致果蝇大脑发生巨大变化;在成年期仍存在的神经元往往会对蜕皮激素ecdysone 做出反应而发生变化。除了驱动重塑,ecdysone 信号还可以改变神经元的分化状态。蘑菇体(MB)Kenyon 细胞的三个连续出生的亚型(γ,其次是α'/β',最后是α/β)作为时间命运的模型。γ神经元也被用作变态期间重塑的模型。由于 γ神经元是幼虫大脑中唯一具有功能的 Kenyon 细胞,因此它们具有所有三种成年亚型的功能。相应地,幼虫 γ神经元的形态与α'/β'和α/β神经元相似-它们的轴突向背部和中部投射。在变态期间,γ神经元重塑形成单个内侧投射。因此,时间命运的改变和重塑缺陷以相似的方式改变 γ神经元的形态。Mamo 是一种广泛复杂、穿越轨道和 bric-à-brac/痘病毒和锌指(BTB/POZ)转录因子,对于α'/β'神经元的时间特异性至关重要,最近被描述为γ重塑所必需。在之前的一项研究中,我们注意到当操纵 mamo 时,表达γ特异性标记的成年 Kenyon 细胞数量发生了变化。这些数据表明 Mamo 在γ神经元命运特化中起作用,但 mamo 直到蛹化期才在 γ神经元中表达,远在 γ特化之后。这表明 mamo 在确保 γ神经元在成年大脑中表达正确的 Kenyon 细胞亚型特异性基因方面具有后期作用。

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