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利用突变多能干细胞对非编码不稳定重复序列扩增疾病进行建模。

Modeling diseases of noncoding unstable repeat expansions using mutant pluripotent stem cells.

作者信息

Yanovsky-Dagan Shira, Mor-Shaked Hagar, Eiges Rachel

机构信息

Shira Yanovsky-Dagan, Hagar Mor-Shaked, Rachel Eiges, Stem Cell Research Laboratory, Medical Genetics Institute, Shaare Zedek Medical Center affiliated with the Hebrew University School of Medicine, Jerusalem 91031, Israel.

出版信息

World J Stem Cells. 2015 Jun 26;7(5):823-38. doi: 10.4252/wjsc.v7.i5.823.

Abstract

Pathogenic mutations involving DNA repeat expansions are responsible for over 20 different neuronal and neuromuscular diseases. All result from expanded tracts of repetitive DNA sequences (mostly microsatellites) that become unstable beyond a critical length when transmitted across generations. Nearly all are inherited as autosomal dominant conditions and are typically associated with anticipation. Pathologic unstable repeat expansions can be classified according to their length, repeat sequence, gene location and underlying pathologic mechanisms. This review summarizes the current contribution of mutant pluripotent stem cells (diseased human embryonic stem cells and patient-derived induced pluripotent stem cells) to the research of unstable repeat pathologies by focusing on particularly large unstable noncoding expansions. Among this class of disorders are Fragile X syndrome and Fragile X-associated tremor/ataxia syndrome, myotonic dystrophy type 1 and myotonic dystrophy type 2, Friedreich ataxia and C9 related amyotrophic lateral sclerosis and/or frontotemporal dementia, Facioscapulohumeral Muscular Dystrophy and potentially more. Common features that are typical to this subclass of conditions are RNA toxic gain-of-function, epigenetic loss-of-function, toxic repeat-associated non-ATG translation and somatic instability. For each mechanism we summarize the currently available stem cell based models, highlight how they contributed to better understanding of the related mechanism, and discuss how they may be utilized in future investigations.

摘要

涉及DNA重复序列扩增的致病性突变与20多种不同的神经和神经肌肉疾病有关。所有这些疾病都是由重复DNA序列(主要是微卫星)的扩增片段引起的,这些片段在世代传递时超过临界长度就会变得不稳定。几乎所有这些疾病都是以常染色体显性遗传病的形式遗传的,并且通常与遗传早现现象有关。病理性不稳定重复序列扩增可根据其长度、重复序列、基因位置和潜在的病理机制进行分类。本综述通过关注特别大的不稳定非编码扩增,总结了突变多能干细胞(患病的人类胚胎干细胞和患者来源的诱导多能干细胞)目前在不稳定重复序列病理学研究中的贡献。这类疾病包括脆性X综合征和脆性X相关震颤/共济失调综合征、1型强直性肌营养不良和2型强直性肌营养不良、弗里德赖希共济失调以及与C9相关的肌萎缩侧索硬化症和/或额颞叶痴呆、面肩肱型肌营养不良,可能还有更多。这类疾病的典型共同特征是RNA毒性功能获得、表观遗传功能丧失、毒性重复相关非ATG翻译和体细胞不稳定性。对于每种机制,我们总结了目前可用的基于干细胞的模型,强调它们如何有助于更好地理解相关机制,并讨论它们在未来研究中可能如何被利用。

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本文引用的文献

1
FMR1 epigenetic silencing commonly occurs in undifferentiated fragile X-affected embryonic stem cells.
Stem Cell Reports. 2014 Nov 11;3(5):699-706. doi: 10.1016/j.stemcr.2014.09.001. Epub 2014 Oct 3.
3
Characterization of the dipeptide repeat protein in the molecular pathogenesis of c9FTD/ALS.
Hum Mol Genet. 2015 Mar 15;24(6):1630-45. doi: 10.1093/hmg/ddu576. Epub 2014 Nov 14.
4
Hypermethylation of repeat expanded C9orf72 is a clinical and molecular disease modifier.
Acta Neuropathol. 2015 Jan;129(1):39-52. doi: 10.1007/s00401-014-1365-0. Epub 2014 Nov 12.
5
7
Clinical and molecular implications of mosaicism in FMR1 full mutations.
Front Genet. 2014 Sep 17;5:318. doi: 10.3389/fgene.2014.00318. eCollection 2014.
8
Abnormalities in human pluripotent cells due to reprogramming mechanisms.
Nature. 2014 Jul 10;511(7508):177-83. doi: 10.1038/nature13551. Epub 2014 Jul 2.
9
Functional characterization of Friedreich ataxia iPS-derived neuronal progenitors and their integration in the adult brain.
PLoS One. 2014 Jul 7;9(7):e101718. doi: 10.1371/journal.pone.0101718. eCollection 2014.
10
Hypermethylation of the CpG-island near the C9orf72 G₄C₂-repeat expansion in FTLD patients.
Hum Mol Genet. 2014 Nov 1;23(21):5630-7. doi: 10.1093/hmg/ddu279. Epub 2014 Jun 6.

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