Department of Neurology, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Neurology. 2010 Jan 19;74(3):229-38. doi: 10.1212/WNL.0b013e3181ca00ca.
THAP1 encodes a transcription factor (THAP1) that harbors an atypical zinc finger domain and regulates cell proliferation. An exon 2 insertion/deletion frameshift mutation in THAP1 is responsible for DYT6 dystonia in Amish-Mennonites. Subsequent screening efforts in familial, mainly early-onset, primary dystonia identified additional THAP1 sequence variants in non-Amish subjects.
To examine a large cohort of subjects with mainly adult-onset primary dystonia for sequence variants in THAP1.
With high-resolution melting, all 3 THAP1 exons were screened for sequence variants in 1,114 subjects with mainly adult-onset primary dystonia, 96 with unclassified dystonia, and 600 controls (400 neurologically normal and 200 with Parkinson disease). In addition, all 3 THAP1 exons were sequenced in 200 subjects with dystonia and 200 neurologically normal controls.
Nine unique melting curves were found in 19 subjects from 16 families with primary dystonia and 1 control. Age at dystonia onset ranged from 8 to 69 years (mean 48 years). Sequencing identified 6 novel missense mutations in conserved regions of THAP1 (G9C [cervical, masticatory, arm], D17G [cervical], F132S [laryngeal], I149T [cervical and generalized], A166T [laryngeal], and Q187K [cervical]). One subject with blepharospasm and another with laryngeal dystonia harbored a c.-42C>T variant. A c.57C>T silent variant was found in 1 subject with segmental craniocervical dystonia. An intron 1 variant (c.71+9C>A) was present in 7 subjects with dystonia (7/1,210) but only 1 control (1/600).
A heterogeneous collection of THAP1 sequence variants is associated with varied anatomical distributions and onset ages of both familial and sporadic primary dystonia.
THAP1 编码一种转录因子(THAP1),其具有非典型锌指结构域,并调节细胞增殖。THAP1 外显子 2 插入/缺失移码突变导致阿米什-门诺派人群中的 DYT6 肌张力障碍。随后在家族性、主要为早发性原发性肌张力障碍患者中进行的筛选工作发现,非阿米什人群中 THAP1 序列变异。
为了研究主要为成年发病的原发性肌张力障碍患者的 THAP1 序列变异。
采用高分辨率熔解曲线法,对 1114 例主要为成年发病的原发性肌张力障碍患者、96 例未分类的肌张力障碍患者和 600 名对照者(400 名神经正常和 200 名帕金森病患者)的 3 个 THAP1 外显子进行序列变异筛查。此外,对 200 例肌张力障碍患者和 200 名神经正常对照者的 3 个 THAP1 外显子进行测序。
在 16 个家族性和 1 个对照组的 19 例原发性肌张力障碍患者中发现了 9 个独特的熔解曲线。肌张力障碍发病年龄为 8-69 岁(平均 48 岁)。测序发现 THAP1 保守区域的 6 个新错义突变(G9C [颈肌、咀嚼肌、臂肌]、D17G [颈肌]、F132S [喉肌]、I149T [颈肌和全身型]、A166T [喉肌]和 Q187K [颈肌])。1 例眼睑痉挛和 1 例喉肌张力障碍患者携带 c.-42C>T 变异。1 例节段性颅颈肌张力障碍患者存在 c.57C>T 沉默变异。1210 例肌张力障碍患者中有 7 例(7/1210)和 600 例对照者中有 1 例(1/600)存在内含子 1 变异(c.71+9C>A)。
THAP1 序列变异的异质性与家族性和散发性原发性肌张力障碍的不同解剖分布和发病年龄有关。