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代森锰在果蝇中诱导多巴胺能神经变性的遗传基础。

Genetic basis of maneb-induced dopaminergic neurodegeneration in Drosophila.

作者信息

Villalobos-Cantor Stefanny, Arreola-Bustos Alicia, Martin Ian

机构信息

Jungers Center for Neurosciences, Department of Neurology, Oregon Health and Science University, Portland, OR 97239, United States.

Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, OR 97239, United States.

出版信息

G3 (Bethesda). 2025 Sep 3;15(9). doi: 10.1093/g3journal/jkaf159.

Abstract

Parkinson's disease (PD) is a complex neurodegenerative disease driven by combined genetic and environmental factors. Human studies support increased PD risk following exposure to the pesticide maneb yet animal studies generally report subtle or no dopaminergic phenotypes unless maneb is combined with additional pesticides. Consequently, it is unclear whether exposure to maneb alone promotes degeneration of dopamine (DA) neurons and if so, what the underlying mechanisms are. We hypothesized that gene-environment interactions are major determinants of maneb-mediated neurodegeneration and in support of this we find that DA neuron viability is divergent among 186 maneb-exposed genetically varying fly strains from the Drosophila Genetic Reference Panel. Through genome-wide association analysis we identify several candidate genetic modifiers of maneb-induced DA neurodegeneration and further validate 2 candidate genes, fz2 and CG14186 which we find potentiate maneb-induced DA neurodegeneration when knocked down. fz2 and the mammalian ortholog of CG14186 (TMEM237) are both thought to be necessary for intact Wnt pathway signaling in nervous system development and maintenance. Accordingly, we find that adult-specific perturbation of Wnt signaling is sufficient to promote maneb-induced DA neuron loss. Collectively, these results support a role for gene-environment interactions in PD etiology and reveal candidate mediators of maneb-related DA neurodegeneration in vivo.

摘要

帕金森病(PD)是一种由遗传和环境因素共同驱动的复杂神经退行性疾病。人体研究表明,接触农药代森锰锌后帕金森病风险增加,但动物研究通常报告,除非代森锰锌与其他农药联合使用,否则不会出现明显的或任何多巴胺能表型。因此,尚不清楚单独接触代森锰锌是否会促进多巴胺(DA)神经元变性,如果会,其潜在机制是什么。我们假设基因 - 环境相互作用是代森锰锌介导的神经变性的主要决定因素,支持这一假设的是,我们发现来自果蝇遗传参考面板的186个暴露于代森锰锌的基因不同的果蝇品系中,DA神经元活力存在差异。通过全基因组关联分析,我们确定了几个代森锰锌诱导的DA神经变性的候选基因修饰因子,并进一步验证了2个候选基因fz2和CG14186,我们发现敲低这两个基因会增强代森锰锌诱导的DA神经变性。fz2和CG14186的哺乳动物直系同源基因(TMEM237)都被认为是神经系统发育和维持中完整Wnt信号通路所必需的。因此,我们发现Wnt信号通路的成年特异性扰动足以促进代森锰锌诱导的DA神经元丢失。总的来说,这些结果支持基因 - 环境相互作用在帕金森病病因学中的作用,并揭示了体内代森锰锌相关DA神经变性的候选介质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30b4/12405872/8e37f903a9b9/jkaf159f1.jpg

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