Department of Biochemistry, The University of Western Ontario, London, Ontario, Canada.
Division of Medical Genetics, Department of Paediatrics, The University of Western Ontario, London, Ontario, Canada.
IUBMB Life. 2024 Dec;76(12):1125-1138. doi: 10.1002/iub.2918. Epub 2024 Oct 1.
Heterozygous pathogenic variants in the histidyl-tRNA synthetase (HARS) gene are associated with Charcot-Marie-Tooth (CMT) type 2W disease, classified as an axonal peripheral neuropathy. To date, at least 60 variants causing CMT symptoms have been identified in seven different aminoacyl-tRNA synthetases, with eight being found in the catalytic domain of HARS. The genetic data clearly show a causative role of aminoacyl-tRNA synthetases in CMT; however, the cellular mechanisms leading to pathology can vary widely and are unknown in the case of most identified variants. Here we describe a novel HARS variant, c.412T>C; p.Y138H, identified through a CMT gene panel in a patient with peripheral neuropathy. To determine the effect of p.Y138H we employed a humanized HARS yeast model and recombinant protein biochemistry, which identified a deficiency in protein dimerization and a growth defect which shows mild but significant improvement with histidine supplementation. This raises the potential for a clinical trial of histidine.
杂合致病性变异位于组氨酰-tRNA 合成酶(HARS)基因中,与 2W 型腓骨肌萎缩症(Charcot-Marie-Tooth,CMT)相关,归类为轴索性周围神经病。迄今为止,已在七种不同的氨酰-tRNA 合成酶中发现了至少 60 种导致 CMT 症状的变异,其中 8 种位于 HARS 的催化结构域中。遗传数据清楚地表明氨酰-tRNA 合成酶在 CMT 中起因果作用;然而,导致病理的细胞机制可能差异很大,而且大多数已确定的变异都未知。在这里,我们描述了一种通过患者周围神经病变的 CMT 基因面板鉴定的新型 HARS 变体 c.412T>C;p.Y138H。为了确定 p.Y138H 的影响,我们使用了人源化 HARS 酵母模型和重组蛋白生物化学,发现其蛋白二聚体缺陷和生长缺陷,而补充组氨酸则显示出轻度但显著的改善。这就提出了进行组氨酸临床试验的可能性。