Parkinson D B, Thakker R V
Division of Molecular Medicine, MRC Clinical Research Centre, Harrow, Middlesex, UK.
Nat Genet. 1992 May;1(2):149-52. doi: 10.1038/ng0592-149.
Investigation of one kindred with autosomal recessive isolated hypoparathyroidism, which had resulted from a consanguineous marriage, has identified a g to c substitution in the first nucleotide of intron 2 of the parathyroid hormone (PTH) gene. This donor splice mutation could be detected by restriction enzyme cleavage with Ddel, and this revealed that the patients were homozygous for the mutant alleles, the unaffected relatives were heterozygous, and unrelated normals were homozygous for the wild type alleles. Defects in messenger RNA splicing were investigated by the detection of illegitimate transcription of the PTH gene in lymphoblastoid cells. The mutation resulted in exon skipping with a loss of exon 2, which encodes the initiation codon and the signal peptide, thereby causing parathyroid hormone deficiency.
对一个因近亲结婚导致常染色体隐性孤立性甲状旁腺功能减退的家族进行研究,已确定甲状旁腺激素(PTH)基因内含子2第一个核苷酸处发生了g到c的替换。这种供体剪接突变可通过用Ddel进行限制性酶切检测到,结果显示患者为突变等位基因的纯合子,未受影响的亲属为杂合子,无关正常人为野生型等位基因的纯合子。通过检测淋巴母细胞中PTH基因的非法转录来研究信使核糖核酸剪接缺陷。该突变导致外显子跳跃,外显子2缺失,外显子2编码起始密码子和信号肽,从而导致甲状旁腺激素缺乏。