双等位基因TSEN2变异导致桥小脑发育不全2型。

IF 2.5 3区 生物学 Q2 GENETICS & HEREDITY
Yukina Hayashi, Keisuke Hamada, Kavitha Rethanavelu, Naomi Tsuchida, Yuri Uchiyama, Eriko Koshimizu, Satoko Miyatake, Takeshi Mizuguchi, Kazuhiro Ogata, Atsushi Fujita, Naomichi Matsumoto
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引用次数: 0

摘要

桥小脑发育不全2型(PCH2)是由tRNA剪接内切酶(TSEN)亚基基因双等位致病变异引起的常染色体隐性神经退行性疾病。TSEN54的变异最为常见,迄今为止报道的与tsen2相关的PCH2B病例很少。在这里,我们报告一个7岁的女孩,具有典型的PCH2特征,包括进行性小头畸形、癫痫、发育迟缓、小脑萎缩和肌张力障碍。外显子组测序显示复合杂合TSEN2变异,已知错义变异NM_025265.4:c。926A>G p.(Tyr309Cys)和新的无义变体c.1048C >t p.(Arg350*)。结构模型表明p.(Tyr309Cys)适度破坏了TSEN2-TSEN54界面的稳定性,而p.(Arg350*)截断了催化结构域。尽管预测p.(Tyr309Cys)对结构的影响很小,但在纯合和复合杂合状态下,p.(Tyr309Cys)都与严重的临床症状相关。本研究扩展了TSEN2突变谱,并强调了将结构建模与临床数据相结合以完善PCH2B基因型-表型相关性的实用性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Biallelic TSEN2 variants causing pontocerebellar hypoplasia type 2.

Pontocerebellar hypoplasia type 2 (PCH2) is an autosomal recessive neurodegenerative disorder caused by biallelic pathogenic variants in tRNA splicing endonuclease (TSEN) subunit genes. Variants in TSEN54 are most common, with very few cases of TSEN2-related PCH2B reported to date. Here, we report a 7-year-old girl with typical PCH2 features, including progressive microcephaly, epilepsy, developmental delay, cerebellar atrophy, and dystonia. Exome sequencing revealed compound heterozygous TSEN2 variants, a known missense variant NM_025265.4:c.926A>G p.(Tyr309Cys) and a novel nonsense variant c.1048C>T p.(Arg350*). Structural modeling suggested that p.(Tyr309Cys) moderately destabilizes the TSEN2-TSEN54 interface, while p.(Arg350*) truncates the catalytic domain. Despite a minor predicted impact on structure, p.(Tyr309Cys) was associated with severe clinical symptoms in both homozygous and compound heterozygous states. This study expands the TSEN2 mutation spectrum and highlights the utility of integrating structural modeling with clinical data to refine genotype-phenotype correlations in PCH2B.

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来源期刊
Journal of Human Genetics
Journal of Human Genetics 生物-遗传学
CiteScore
7.20
自引率
0.00%
发文量
101
审稿时长
4-8 weeks
期刊介绍: The Journal of Human Genetics is an international journal publishing articles on human genetics, including medical genetics and human genome analysis. It covers all aspects of human genetics, including molecular genetics, clinical genetics, behavioral genetics, immunogenetics, pharmacogenomics, population genetics, functional genomics, epigenetics, genetic counseling and gene therapy. Articles on the following areas are especially welcome: genetic factors of monogenic and complex disorders, genome-wide association studies, genetic epidemiology, cancer genetics, personal genomics, genotype-phenotype relationships and genome diversity.
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