Hayashi Yukina, Hamada Keisuke, Rethanavelu Kavitha, Tsuchida Naomi, Uchiyama Yuri, Koshimizu Eriko, Miyatake Satoko, Mizuguchi Takeshi, Ogata Kazuhiro, Fujita Atsushi, Matsumoto Naomichi
Department of Human Genetics, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Department of Biochemistry, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
J Hum Genet. 2025 Aug 27. doi: 10.1038/s10038-025-01393-3.
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.
2型脑桥小脑发育不全(PCH2)是一种常染色体隐性神经退行性疾病,由tRNA剪接内切酶(TSEN)亚基基因的双等位基因致病性变异引起。TSEN54的变异最为常见,迄今为止,报道的与TSEN2相关的PCH2B病例非常少。在此,我们报告一名7岁女孩,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。外显子组测序揭示了复合杂合性TSEN2变异,一个已知的错义变异NM_025265.4:c.926A>G p.(Tyr309Cys)和一个新的无义变异c.1048C>T p.(Arg350*)。结构建模表明,p.(Tyr309Cys)会适度破坏TSEN2-TSEN54界面的稳定性,而p.(Arg350*)会截断催化结构域。尽管对结构的预测影响较小,但p.(Tyr309Cys)在纯合和复合杂合状态下均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。