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遗传基因研究揭示了脑静脉畸形 2 基因中的一个缺失突变。

Genetic genealogy uncovers a founder deletion mutation in the cerebral cavernous malformations 2 gene.

机构信息

Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC, 27710, USA.

Angioma Alliance, Charlottesville, VA, 22901, USA.

出版信息

Hum Genet. 2022 Nov;141(11):1761-1769. doi: 10.1007/s00439-022-02458-5. Epub 2022 Apr 30.

Abstract

Cerebral cavernous malformations (CCM) are vascular malformations consisting of collections of enlarged capillaries occurring in the brain or spinal cord. These vascular malformations can occur sporadically or susceptibility to develop these can be inherited as an autosomal dominant trait due to mutation in one of three genes. Over a decade ago, we described a 77.6 Kb germline deletion spanning exons 2-10 in the CCM2 gene found in multiple affected individuals from seemingly unrelated families. Segregation analysis using linked, microsatellite markers indicated that this deletion may have arisen at least twice independently. In the ensuing decades, many more CCM patients have been identified with this deletion. In this present study we examined 27 reportedly unrelated affected individuals with this deletion. To investigate the origin of the deletion at base pair level resolution, we sequenced approximately 10 Kb upstream and downstream from the recombination junction on the deleted allele. All patients showed the identical SNP haplotype across this combined 20 Kb interval. In parallel, genealogical records have traced 11 of these individuals to five separate pedigrees dating as far back as the 1600-1700s. These haplotype and genealogical data suggest that these families and the remaining "unrelated" samples converge on a common ancestor due to a founder mutation occurring centuries ago on the North American continent. We also note that another gene, NACAD, is included in this deletion. Although patient self-reporting does not indicate an apparent phenotypic consequence for heterozygous deletion of NACAD, further investigation is warranted for these patients.

摘要

脑内海绵状血管畸形(CCM)是由脑或脊髓中扩张的毛细血管集合而成的血管畸形。这些血管畸形可以是散发性的,也可以是由于三个基因之一的突变而遗传的常染色体显性遗传特征。十多年前,我们描述了一种 77.6kb 的种系缺失,跨越 CCM2 基因的外显子 2-10,在来自看似无关的多个家族的多个受影响个体中发现。使用连锁微卫星标记的分离分析表明,这种缺失可能至少独立发生了两次。在随后的几十年里,发现了更多患有这种缺失的 CCM 患者。在本研究中,我们检查了 27 名据报道患有这种缺失的无关受影响个体。为了在碱基对分辨率水平上研究缺失的起源,我们对缺失等位基因上重组连接点上下游约 10kb 进行了测序。所有患者在这 20kb 间隔的共同区域都显示出相同的 SNP 单倍型。同时,系谱记录追溯到这些个体中的 11 人,他们来自五个独立的家谱,最早可以追溯到 17 世纪。这些单倍型和系谱数据表明,这些家族和其余的“无关”样本由于几个世纪前在北美大陆发生的创始突变而汇聚到一个共同的祖先。我们还注意到,另一个基因 NACAD 也包含在这个缺失中。尽管患者的自我报告表明 NACAD 杂合缺失没有明显的表型后果,但这些患者仍需要进一步调查。

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