谷胱甘肽s -转移酶的敲低导致cabeza在大脑中的错误定位和积累,cabeza是果蝇FUS的同源物。

IF 1.8 4区 医学 Q3 GENETICS & HEREDITY Journal of neurogenetics Pub Date : 2023-03-01 DOI:10.1080/01677063.2022.2149747
Sun Joo Cha, Ja Hoon Yoon, Yeo Jeong Han, Kiyoung Kim
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引用次数: 2

摘要

谷胱甘肽s -转移酶(GSTO)是一种抗氧化酶,参与减少氧化应激。最近的研究表明,GSTOs的多态性变异影响神经退行性疾病的发病年龄和进展。虽然GSTO活性可能影响多种疾病的发展和年龄依赖性,但神经元中GSTO失活调控神经退行性疾病易感性的机制尚不清楚。在本研究中,果蝇中GstO2的敲低导致神经元中Cabeza (Caz)蛋白水平以年龄依赖的方式增加。Caz果蝇是人类FUS的同源基因,它与神经退行性疾病有关,包括肌萎缩侧索硬化症(ALS)和额颞叶痴呆(FTD)。我们发现GstO2敲除后神经元胞质Caz错定位和聚集显著增加。GstO2的下调降低了老化神经元中Caz蛋白的溶解度。这些发现表明GSTO通过调节果蝇神经系统中Caz的定位和聚集,是神经退行性疾病发展的重要调节剂。
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Knockdown of glutathione S-transferase leads to mislocalization and accumulation of cabeza, a drosophila homolog of FUS, in the brain.

Glutathione S-transferase omega (GSTO) is an antioxidant enzyme involved in reducing oxidative stress. Recent studies suggest that polymorphic variants of GSTOs affect the onset age and progression of neurodegenerative diseases. Although GSTO activity may affect the development and age dependency of several diseases, the mechanism by which GSTO inactivation in neurons regulates the susceptibility to neurodegenerative diseases is unclear. In the present study, GstO2 knockdown in Drosophila led to increased levels of Cabeza (Caz) protein in neurons in an age-dependent manner. Drosophila Caz is the ortholog of human FUS, which is associated with neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). We found that cytoplasmic Caz mislocalization and aggregation in neurons significantly increased after GstO2 knockdown in vivo. Downregulation of GstO2 decreased the solubility of the Caz protein in aging neurons. These findings demonstrate that GSTO is a critical modulator of the development of neurodegenerative diseases by regulating Caz localization and aggregation in the nervous system of Drosophila.

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来源期刊
Journal of neurogenetics
Journal of neurogenetics 医学-神经科学
CiteScore
4.40
自引率
0.00%
发文量
13
审稿时长
>12 weeks
期刊介绍: The Journal is appropriate for papers on behavioral, biochemical, or cellular aspects of neural function, plasticity, aging or disease. In addition to analyses in the traditional genetic-model organisms, C. elegans, Drosophila, mouse and the zebrafish, the Journal encourages submission of neurogenetic investigations performed in organisms not easily amenable to experimental genetics. Such investigations might, for instance, describe behavioral differences deriving from genetic variation within a species, or report human disease studies that provide exceptional insights into biological mechanisms
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