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高尔基氏体的结构不受与肌张力障碍相关基因 Tor1a 中 GAG 缺失突变的影响。

Structure of the Golgi apparatus is not influenced by a GAG deletion mutation in the dystonia-associated gene Tor1a.

机构信息

Department of Molecular Physiology and Biophysics, University of Iowa Carver College of Medicine, Iowa City, Iowa, United States of America.

Department of Chemical and Biochemical Engineering, University of Iowa College of Engineering, Iowa City, Iowa, United States of America.

出版信息

PLoS One. 2018 Nov 7;13(11):e0206123. doi: 10.1371/journal.pone.0206123. eCollection 2018.

Abstract

Autosomal-dominant, early-onset DYT1 dystonia is associated with an in-frame deletion of a glutamic acid codon (ΔE) in the TOR1A gene. The gene product, torsinA, is an evolutionarily conserved AAA+ ATPase. The fact that constitutive secretion from patient fibroblasts is suppressed indicates that the ΔE-torsinA protein influences the cellular secretory machinery. However, which component is affected remains unclear. Prompted by recent reports that abnormal protein trafficking through the Golgi apparatus, the major protein-sorting center of the secretory pathway, is sometimes associated with a morphological change in the Golgi, we evaluated the influence of ΔE-torsinA on this organelle. Specifically, we examined its structure by confocal microscopy, in cultures of striatal, cerebral cortical and hippocampal neurons obtained from wild-type, heterozygous and homozygous ΔE-torsinA knock-in mice. In live neurons, the Golgi was assessed following uptake of a fluorescent ceramide analog, and in fixed neurons it was analyzed by immuno-fluorescence staining for the Golgi-marker GM130. Neither staining method indicated genotype-specific differences in the size, staining intensity, shape or localization of the Golgi. Moreover, no genotype-specific difference was observed as the neurons matured in vitro. These results were supported by a lack of genotype-specific differences in GM130 expression levels, as assessed by Western blotting. The Golgi was also disrupted by treatment with brefeldin A, but no genotype-specific differences were found in the immuno-fluorescence staining intensity of GM130. Overall, our results demonstrate that the ΔE-torsinA protein does not drastically influence Golgi morphology in neurons, irrespective of genotype, brain region (among those tested), or maturation stage in culture. While it remains possible that functional changes in the Golgi exist, our findings imply that any such changes are not severe enough to influence its morphology to a degree detectable by light microscopy.

摘要

常染色体显性遗传,早发性 DYT1 肌张力障碍与 TOR1A 基因中谷氨酸密码子(ΔE)的框内缺失有关。该基因产物 torsinA 是一种进化上保守的 AAA+ATP 酶。从患者成纤维细胞中持续分泌受到抑制的事实表明,ΔE-torsinA 蛋白影响细胞分泌机制。然而,哪种成分受到影响尚不清楚。最近有报道称,高尔基体(细胞分泌途径的主要蛋白质分拣中心)中异常蛋白质运输有时与高尔基体形态改变有关,受此启发,我们评估了ΔE-torsinA 对该细胞器的影响。具体而言,我们使用共聚焦显微镜在从野生型、杂合子和纯合子ΔE-torsinA 基因敲入小鼠中获得的纹状体、大脑皮质和海马神经元培养物中检查其结构。在活神经元中,通过摄取荧光神经酰胺类似物评估高尔基体,并用 GM130 免疫荧光染色固定神经元分析高尔基体。两种染色方法均未显示出基因型特异性的高尔基体大小、染色强度、形状或定位差异。此外,在体外神经元成熟过程中也未观察到基因型特异性差异。Western 印迹分析 GM130 表达水平也支持没有基因型特异性差异。用布雷菲德菌素 A 处理也会破坏高尔基体,但 GM130 的免疫荧光染色强度没有基因型特异性差异。总体而言,我们的结果表明,ΔE-torsinA 蛋白不会极大地影响神经元中的高尔基体形态,无论基因型、脑区(在所测试的脑区中)或培养物中的成熟阶段如何。虽然高尔基体的功能变化仍然存在,但我们的发现表明,任何此类变化都不足以影响其形态,无法通过光镜检测到。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daf7/6221310/a238879a180e/pone.0206123.g012.jpg

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