神经胶质过氧化物酶体功能障碍诱发果蝇轴突肿胀和神经炎症

IF 2.1 3区 生物学 Q3 GENETICS & HEREDITY G3: Genes|Genomes|Genetics Pub Date : 2024-10-10 DOI:10.1093/g3journal/jkae243
Maggie Sodders, Anurag Das, Hua Bai
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摘要

众所周知,神经胶质细胞可通过神经胶质细胞与神经元之间的通讯影响神经元的功能。本研究以果蝇神经肌肉接头(NMJ)为模型系统,旨在阐明过氧化物酶体介导的神经胶质细胞-神经元通讯的机制。我们在成年果蝇的腹部 NMJ 中观察到了高丰度的过氧物酶体。有趣的是,胶质细胞特异性敲除过氧异构体导入受体蛋白Pex5会显著增加轴突面积和体积,并导致轴突肿胀。轴突结构的扩大很可能是有害的,因为胶团特异性敲除Pex5的果蝇表现出年龄依赖性运动缺陷。此外,神经胶质细胞过氧异构体醚脂生物合成障碍也会导致轴突肿胀。与我们之前的研究一致,过氧物酶体导入功能缺陷会上调神经胶质细胞中的促炎细胞因子upd3,而神经胶质细胞特异性过表达upd3会诱导轴突肿胀。此外,运动神经元特异性地通过hop过表达激活JAK-STAT通路也会导致轴突肿胀。我们的研究结果表明,神经胶质过氧物酶体受损会改变轴突形态、神经炎症和运动神经元功能。
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Glial peroxisome dysfunction induces axonal swelling and neuroinflammation in Drosophila.

Glial cells are known to influence neuronal functions through glia-neuron communication. The present study aims to elucidate the mechanism behind peroxisome-mediated glia-neuron communication using Drosophila neuromuscular junction (NMJ) as a model system. We observe a high abundance of peroxisomes in the abdominal NMJ of adult Drosophila. Interestingly, glia-specific knockdown of peroxisome import receptor protein, Pex5, significantly increases axonal area and volume and leads to axon swelling. The enlarged axonal structure is likely deleterious, as the flies with glia-specific knockdown of Pex5 exhibit age-dependent locomotion defects. In addition, impaired peroxisomal ether lipid biosynthesis in glial cells also induces axon swelling. Consistent with our previous work, defective peroxisomal import function upregulates pro-inflammatory cytokine upd3 in glial cells, while glia-specific overexpression of upd3 induces axonal swelling. Furthermore, motor neuron-specific activation of the JAK-STAT pathway through hop overexpression results in axon swelling. Our findings demonstrated that impairment of glial peroxisomes alters axonal morphology, neuroinflammation, and motor neuron function.

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来源期刊
G3: Genes|Genomes|Genetics
G3: Genes|Genomes|Genetics GENETICS & HEREDITY-
CiteScore
5.10
自引率
3.80%
发文量
305
审稿时长
3-8 weeks
期刊介绍: G3: Genes, Genomes, Genetics provides a forum for the publication of high‐quality foundational research, particularly research that generates useful genetic and genomic information such as genome maps, single gene studies, genome‐wide association and QTL studies, as well as genome reports, mutant screens, and advances in methods and technology. The Editorial Board of G3 believes that rapid dissemination of these data is the necessary foundation for analysis that leads to mechanistic insights. G3, published by the Genetics Society of America, meets the critical and growing need of the genetics community for rapid review and publication of important results in all areas of genetics. G3 offers the opportunity to publish the puzzling finding or to present unpublished results that may not have been submitted for review and publication due to a perceived lack of a potential high-impact finding. G3 has earned the DOAJ Seal, which is a mark of certification for open access journals, awarded by DOAJ to journals that achieve a high level of openness, adhere to Best Practice and high publishing standards.
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