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错义突变使遗传性进行性肌张力障碍中的鸟苷三磷酸环化水解酶I失活。

Missense mutants inactivate guanosine triphosphate cyclohydrolase I in hereditary progressive dystonia.

作者信息

Ueno S, Hirano M

机构信息

Department of Medical Genetics, Nara Medical University, Shijo-cho 840, Kashihara, 634-8521, Nara, Japan.

出版信息

Brain Dev. 2000 Sep;22 Suppl 1:S111-4. doi: 10.1016/s0387-7604(00)00135-2.

Abstract

Hereditary progressive dystonia (HPD) with marked diurnal fluctuation is caused by mutant guanosine triphosphate (GTP) cyclohydrolase I (GCH). The clinical presentation of dominant HPD varies considerably. We proposed the hypothesis that a relative increase of mutant GCH capable of inhibiting normal GCH is responsible for heterogeneous phenotypic manifestations. In a Japanese family with a novel G90V mutation, an affected heterozygote had a higher mutant/normal mRNA ratio than an unaffected heterozygote. Co-expression analysis showed that mutant enzyme (GCH-G90V) inactivated the normal enzyme in the COS cells. Similarly, GCH-G203R showed the dominant negative effects. These results supported our proposed hypothesis.

摘要

伴有明显昼夜波动的遗传性进行性肌张力障碍(HPD)由突变的鸟苷三磷酸(GTP)环化水解酶I(GCH)引起。显性HPD的临床表现差异很大。我们提出了一个假说,即能够抑制正常GCH的突变GCH相对增加是导致异质性表型表现的原因。在一个具有新型G90V突变的日本家族中,一名受影响的杂合子的突变/正常mRNA比值高于未受影响的杂合子。共表达分析表明,突变酶(GCH-G90V)在COS细胞中使正常酶失活。同样,GCH-G203R也显示出显性负效应。这些结果支持了我们提出的假说。

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