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基于微阵列的纯合性映射鉴定肾脏-肝脏-胰腺发育不良的基因。

Identification of a gene for renal-hepatic-pancreatic dysplasia by microarray-based homozygosity mapping.

机构信息

Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, N-5021 Bergen, Norway.

出版信息

J Mol Diagn. 2010 Jan;12(1):125-31. doi: 10.2353/jmoldx.2010.090033. Epub 2009 Dec 10.

Abstract

We have investigated a family where two siblings had a developmental disorder associated with polycystic dysplastic kidney disease that was incompatible with postnatal survival. Additional features observed were ductal plate malformation in the liver, dysplasia of the pancreas, and (in one individual) complete situs inversus and polymicrogyria of the cingulate gyri. The autopsy findings were compatible with renal-hepatic-pancreatic dysplasia, a condition with unknown genetic cause at the time of autopsy but with similarities to the Meckel-Gruber/Joubert group of recessive ciliopathies. Consanguinity between the parents made it likely that the mutated gene (with known or potential function in cilia) was located within a rather large region of homozygosity in the affected individuals (identical by descent). Using genetic markers (50K single nucleotide polymorphism microarrays), we found a single large homozygous region of 21.16 Mb containing approximately 200 genes on the long arm of chromosome 3. This region contained two known ciliopathy genes: NPHP3 (adolescent nephronophthisis) and IQCB1 (NPHP5), which is associated with Senior-Löken syndrome. In NPHP3, homozygosity for a deletion of the conserved splice acceptor dinucleotide (AG) preceding exon 20 was found. Our finding confirms the recent report that NPHP3-null mutations cause renal-hepatic-pancreatic dysplasia. Also, our case illustrates that genes for rare and genetically heterogeneous recessive conditions may be identified by homozygosity mapping using single nucleotide polymorphism arrays in the routine clinical setting.

摘要

我们研究了一个家系,该家系中有两名患有与多囊性发育不良性肾疾病相关的发育障碍的兄弟姐妹,这种疾病在出生后无法存活。观察到的其他特征是肝脏的胆管板畸形、胰腺发育不良以及(在一个个体中)完全内脏反转和扣带回的脑回多微小脑回。尸检结果与肝肾胰发育不良一致,在尸检时这种疾病的遗传原因未知,但与隐性纤毛病的 Meckel-Gruber/Joubert 组有相似之处。父母之间的近亲关系使得受影响个体(同源同代)中突变基因(已知或潜在功能在纤毛中)位于相当大的纯合区域内的可能性增加。使用遗传标记(50K 单核苷酸多态性微阵列),我们发现了一个长 3 号染色体上的 21.16Mb 的单一大型纯合区域,该区域包含大约 200 个基因。该区域包含两个已知的纤毛病基因:NPHP3(青少年型肾单位肾痨病)和 IQCB1(NPHP5),后者与 Senior-Löken 综合征相关。在 NPHP3 中,发现了第 20 外显子前保守剪接受体二核苷酸(AG)缺失的纯合性。我们的发现证实了最近的报告,即 NPHP3 基因突变导致肝肾胰发育不良。此外,我们的病例表明,使用单核苷酸多态性阵列进行纯合性作图可以在常规临床环境中鉴定出罕见和遗传异质性隐性疾病的基因。

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