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家族性中枢性尿崩症中精氨酸加压素-神经垂体素II基因新突变的鉴定。

Identification of a novel mutation in the arginine vasopressin-neurophysin II gene in familial central diabetes insipidus.

作者信息

Bullmann C, Kotzka J, Grimm T, Heppner C, Jockenhövel F, Krone W, Müller-Wieland D

机构信息

Medical Clinic II and at the Center for Molecular Medicine, University of Cologne, Germany.

出版信息

Exp Clin Endocrinol Diabetes. 2002 May;110(3):134-7. doi: 10.1055/s-2002-29091.

Abstract

Familial central diabetes insipidus is an inherited disease of predominant autosomal dominant trait characterized by a deficiency of arginine vasopressin. The arginine vasopressin-neurophysin II ( AVP-NPII) gene consists of three exons and is located on chromosome 20p13 encoding for the precursor protein of AVP. We investigated two Caucasian families with a typical autosomal dominant trait of familial central diabetes insipidus, defined by deficiency of arginine vasopressin. After PCR amplification of exon 1 and exon 2/3, fragments were pooled and purified. Nucleotide sequencing was performed with the Taq DyeDeoxy-terminator cycle sequencing method using nested primers. Two mutations in the coding region of NPII were identified. In family C we found a heterozygous G ==> C missense mutation (AA61) in exon 2 leading to the substitution of cystein with serine. In family D a novel heterozygous nonsense mutation in exon 3 (AA 83, GAG ==> TAG) was indentified, leading to a stop codon instead of glutamine. Both mutations were confirmed by restriction analysis and were found in all affected but not in healthy family members or control subjects. We therefore have identified a missense mutation of the AVP-NPII gene and a novel mutation predicting a truncated protein.

摘要

家族性中枢性尿崩症是一种以精氨酸加压素缺乏为特征的、主要呈常染色体显性遗传的疾病。精氨酸加压素-神经垂体素II(AVP-NPII)基因由三个外显子组成,位于20号染色体p13上,编码AVP的前体蛋白。我们研究了两个具有家族性中枢性尿崩症典型常染色体显性特征的白种人家庭,该疾病由精氨酸加压素缺乏所定义。对外显子1和外显子2/3进行PCR扩增后,将片段合并并纯化。使用巢式引物,采用Taq DyeDeoxy-终止循环测序法进行核苷酸测序。在NPII的编码区鉴定出两个突变。在C家族中,我们在外显子2中发现了一个杂合的G ==> C错义突变(AA61),导致半胱氨酸被丝氨酸取代。在D家族中,在外显子3中鉴定出一个新的杂合无义突变(AA 83,GAG ==> TAG),导致产生一个终止密码子而非谷氨酰胺。这两个突变均通过限制性分析得到证实,且在所有患病家庭成员中发现,而在健康家庭成员或对照受试者中未发现。因此,我们鉴定出了AVP-NPII基因的一个错义突变以及一个预测会产生截短蛋白的新突变。

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