Hemanth Tummala, Amanda J Walne, Mohsin Badat, Manthan Patel, Abigail M Walne, Jenna Alnajar, Chi Ching Chow, Ibtehal Albursan, Jennifer M Frost, David Ballard, Sally Killick, Peter Szitányi, Anne M Kelly, Manoj Raghavan, Corrina Powell, Reinier Raymakers, Tony Todd, Elpis Mantadakis, Sophia Polychronopoulou, Nikolas Pontikos, Tianyi Liao, Pradeep Madapura, Upal Hossain, Tom Vulliamy, Inderjeet Dokal
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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. 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引用次数: 0
摘要
先天性角化不良症(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% 的病例在基因水平上仍未定性。为了探索遗传特征,我们对大量临床诊断的DC病例以及表现出类似DC特征的病例(被称为 "类DC"(DCL))进行了遗传研究。这使我们在已知基因位点和新型 X 连锁基因 POLA1 中发现了几个新的致病变体。此外,我们还在不同家族的多个病例中发现了 POT1 和 ZCCHC8 的几个新型变体,从而扩大了 DC 和 DCL 表型的等位基因系列。对新型 POLA1 和 POT1 变体的功能特性分析表明,这些变体对与引物酶、CTC1-STN1-TEN1(CST)和庇护素亚基复合物的蛋白-蛋白相互作用有致病作用,而蛋白-蛋白相互作用对端粒的维持至关重要。ZCCHC8变体显示了ZCCHC8缺乏和普遍转录的迹象,引发了患者血液中的炎症。总之,我们的研究扩展了当前的遗传结构,并拓宽了我们对DC和DCL疾病机制的理解。
The evolving genetic landscape of telomere biology disorder dyskeratosis congenita.
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.
期刊介绍:
EMBO Molecular Medicine is an open access journal in the field of experimental medicine, dedicated to science at the interface between clinical research and basic life sciences. In addition to human data, we welcome original studies performed in cells and/or animals provided they demonstrate human disease relevance.
To enhance and better specify our commitment to precision medicine, we have expanded the scope of EMM and call for contributions in the following fields:
Environmental health and medicine, in particular studies in the field of environmental medicine in its functional and mechanistic aspects (exposome studies, toxicology, biomarkers, modeling, and intervention).
Clinical studies and case reports - Human clinical studies providing decisive clues how to control a given disease (epidemiological, pathophysiological, therapeutic, and vaccine studies). Case reports supporting hypothesis-driven research on the disease.
Biomedical technologies - Studies that present innovative materials, tools, devices, and technologies with direct translational potential and applicability (imaging technologies, drug delivery systems, tissue engineering, and AI)