通过突变分析产前排除ehers - danlos综合征VI型。

H N Yeowell, L C Walker
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引用次数: 12

摘要

我们通过筛选胎儿DNA中的lysyl羟化酶(LH)基因突变,对一个患有ehers - danlos综合征VI型(EDS VI)(一种遗传性胶原蛋白疾病)的家庭进行了首次临床表型产前评估。我们以前报道过,该家庭的患儿是LH基因突变的复合杂合。一个等位基因具有父亲遗传的C1557到G的变化,编码14外显子的过早终止密码子(Y511X),另一个等位基因具有外显子5的缺失,这是由于5内含子一致供体剪接位点的母亲遗传突变造成的。为了进行产前诊断,我们对从妊娠10周培养的绒毛膜绒毛细胞中分离的基因组DNA进行测序。其中一个等位基因在第5外显子剪接位点发生母系遗传的gt ->突变,而另一个等位基因是正常的。由于EDS VI是一种隐性疾病,我们预测虽然是携带者,但婴儿应该不会受到影响。这一结论得到了绒毛膜绒毛细胞中黄体生成素活性正常水平的支持,并被一个健康的未受影响婴儿的出生所证实。
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Prenatal exclusion of Ehlers-Danlos syndrome type VI by mutational analysis.

We have performed the first prenatal assessment of clinical phenotype in a family affected by Ehlers-Danlos syndrome type VI (EDS VI), an inherited collagen disorder, by screening the fetal DNA for mutations in the lysyl hydroxylase (LH) gene. We have previously reported that the affected child in this family is compound heterozygous for mutations in the LH gene. One allele has a paternally inherited C1557 to G change that codes for a premature stop codon (Y511X) in exon 14 and the other allele has a deletion of exon 5 that results from a maternally inherited mutation in the consensus donor splice site of intron 5. To perform the prenatal diagnosis, we sequenced genomic DNA isolated from cultured chorionic villus cells at 10 weeks of gestation. One allele had the maternally inherited gt --> at splice-site mutation in exon 5, and the other paternally inherited allele was normal. As EDS VI is a recessive disorder, we predicted that although a carrier, the baby should be unaffected. This conclusion, which was supported by a normal level of LH activity in the chorionic villus cells, was confirmed by the birth of a healthy unaffected baby.

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