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端粒生物学障碍先天性角化不良的不断演变的遗传景观。

The evolving genetic landscape of telomere biology disorder dyskeratosis congenita.

机构信息

Centre for Genomics and Child Health, Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, Newark Street, London, E12AT, UK.

Barts Health NHS Trust, London, UK.

出版信息

EMBO Mol Med. 2024 Oct;16(10):2560-2582. doi: 10.1038/s44321-024-00118-x. Epub 2024 Aug 28.

Abstract

Dyskeratosis congenita (DC) is a rare inherited bone marrow failure syndrome, caused by genetic mutations that principally affect telomere biology. Approximately 35% of cases remain uncharacterised at the genetic level. To explore the genetic landscape, we conducted genetic studies on a large collection of clinically diagnosed cases of DC as well as cases exhibiting features resembling DC, referred to as 'DC-like' (DCL). This led us to identify several novel pathogenic variants within known genetic loci and in the novel X-linked gene, POLA1. In addition, we have also identified several novel variants in POT1 and ZCCHC8 in multiple cases from different families expanding the allelic series of DC and DCL phenotypes. Functional characterisation of novel POLA1 and POT1 variants, revealed pathogenic effects on protein-protein interactions with primase, CTC1-STN1-TEN1 (CST) and shelterin subunit complexes, that are critical for telomere maintenance. ZCCHC8 variants demonstrated ZCCHC8 deficiency and signs of pervasive transcription, triggering inflammation in patients' blood. In conclusion, our studies expand the current genetic architecture and broaden our understanding of disease mechanisms underlying DC and DCL disorders.

摘要

先天性角化不良(DC)是一种罕见的遗传性骨髓衰竭综合征,由主要影响端粒生物学的基因突变引起。大约 35%的病例在遗传水平上仍未得到明确表征。为了探索遗传图谱,我们对大量临床诊断为 DC 的病例以及表现出类似于 DC 的特征的病例(称为“DC 样”(DCL))进行了遗传研究。这导致我们在已知遗传基因座和新型 X 连锁基因 POLA1 内发现了几个新的致病性变异体。此外,我们还在来自不同家族的多个病例中发现了 POT1 和 ZCCHC8 中的几个新变体,扩展了 DC 和 DCL 表型的等位基因系列。对新型 POLA1 和 POT1 变体的功能特征进行了分析,揭示了它们对与引发蛋白-蛋白相互作用的影响,这些蛋白-蛋白相互作用对于端粒维持至关重要,包括引发酶、CTC1-STN1-TEN1(CST)和庇护素亚基复合物。ZCCHC8 变体表现出 ZCCHC8 缺乏和普遍转录的迹象,在患者的血液中引发炎症。总之,我们的研究扩展了当前的遗传结构,并加深了我们对 DC 和 DCL 疾病机制的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b47/11473520/3e3f54481242/44321_2024_118_Fig1_HTML.jpg

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