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非洲血统神经退行性疾病风险变异破坏了GBA1基因的一个内含子分支点。

African ancestry neurodegeneration risk variant disrupts an intronic branchpoint in GBA1.

作者信息

Álvarez Jerez Pilar, Wild Crea Peter, Ramos Daniel M, Gustavsson Emil K, Radefeldt Mandy, Damianov Andrey, Makarious Mary B, Ojo Oluwadamilola O, Billingsley Kimberley J, Malik Laksh, Daida Kensuke, Bromberek Sarah, Hu Fangle, Schneider Zachary, Surapaneni Aditya L, Stadler Julia, Rizig Mie, Morris Huw R, Pantazis Caroline B, Leonard Hampton L, Screven Laurel, Qi Yue A, Nalls Mike A, Bandres-Ciga Sara, Hardy John, Houlden Henry, Eng Celeste, Burchard Esteban González, Kachuri Linda, Lin Chia-Ho, Black Douglas L, Singleton Andrew B, Fischer Steffen, Bauer Peter, Reed Xylena, Ryten Mina, Beetz Christian, Ward Michael, Okubadejo Njideka U, Blauwendraat Cornelis

机构信息

Center for Alzheimer's and Related Dementias, National Institute on Aging and National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.

Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA.

出版信息

Nat Struct Mol Biol. 2024 Dec;31(12):1955-1963. doi: 10.1038/s41594-024-01423-2. Epub 2024 Dec 12.

Abstract

Recently, an African ancestry-specific Parkinson disease (PD) risk signal was identified at the gene encoding glucocerebrosidase (GBA1). This variant ( rs3115534 -G) is carried by ~50% of West African PD cases and imparts a dose-dependent increase in risk for disease. The risk variant has varied frequencies across African ancestry groups but is almost absent in European and Asian ancestry populations. GBA1 is a gene of high clinical and therapeutic interest. Damaging biallelic protein-coding variants cause Gaucher disease and monoallelic variants confer risk for PD and dementia with Lewy bodies, likely by reducing the function of glucocerebrosidase. Interestingly, the African ancestry-specific GBA1 risk variant is a noncoding variant, suggesting a different mechanism of action. Using full-length RNA transcript sequencing, we identified partial intron 8 expression in risk variant carriers (G) but not in nonvariant carriers (T). Antibodies targeting the N terminus of glucocerebrosidase showed that this intron-retained isoform is likely not protein coding and subsequent proteomics did not identify a shorter protein isoform, suggesting that the disease mechanism is RNA based. Clustered regularly interspaced short palindromic repeats editing of the reported index variant ( rs3115534 ) revealed that this is the sequence alteration responsible for driving the production of these transcripts containing intron 8. Follow-up analysis of this variant showed that it is in a key intronic branchpoint sequence and, therefore, has important implications in splicing and disease. In addition, when measuring glucocerebrosidase activity, we identified a dose-dependent reduction in risk variant carriers. Overall, we report the functional effect of a GBA1 noncoding risk variant, which acts by interfering with the splicing of functional GBA1 transcripts, resulting in reduced protein levels and reduced glucocerebrosidase activity. This understanding reveals a potential therapeutic target in an underserved and underrepresented population.

摘要

最近,在编码葡糖脑苷脂酶(GBA1)的基因上发现了一个特定于非洲血统的帕金森病(PD)风险信号。这种变异(rs3115534 -G)在约50%的西非PD病例中存在,并使疾病风险呈剂量依赖性增加。该风险变异在不同非洲血统群体中的频率有所不同,但在欧洲和亚洲血统人群中几乎不存在。GBA1是一个具有高度临床和治疗意义的基因。有害的双等位基因蛋白质编码变异会导致戈谢病,单等位基因变异会增加患PD和路易体痴呆的风险,可能是通过降低葡糖脑苷脂酶的功能。有趣的是,特定于非洲血统的GBA1风险变异是一个非编码变异,提示了一种不同的作用机制。通过全长RNA转录本测序,我们在风险变异携带者(G)中鉴定出部分内含子8表达,而在非变异携带者(T)中未发现。针对葡糖脑苷脂酶N端的抗体显示,这种保留内含子的异构体可能不编码蛋白质,随后的蛋白质组学也未鉴定出较短的蛋白质异构体,这表明疾病机制是基于RNA的。对报告的索引变异(rs3115534)进行成簇规律间隔短回文重复序列编辑显示,这种序列改变是驱动这些包含内含子8的转录本产生的原因。对该变异的后续分析表明,它位于一个关键的内含子分支点序列中,因此对剪接和疾病具有重要意义。此外,在测量葡糖脑苷脂酶活性时,我们在风险变异携带者中发现了剂量依赖性降低。总体而言,我们报告了一个GBA1非编码风险变异的功能效应,它通过干扰功能性GBA1转录本的剪接起作用,导致蛋白质水平降低和葡糖脑苷脂酶活性降低。这一认识揭示了一个在服务不足和代表性不足人群中的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc80/11638064/0c34daed92ff/41594_2024_1423_Fig1_HTML.jpg

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