| Literature DB >> 28369220 |
Pei-Chien Tsai1,2,3, Bing-Wen Soong1,2,3,4, Inès Mademan5,6, Yen-Hua Huang7,8, Chia-Rung Liu9, Cheng-Tsung Hsiao1,2, Hung-Ta Wu1,10, Tze-Tze Liu11, Yo-Tsen Liu1,2, Yen-Ting Tseng1,2, Kon-Ping Lin1,2, Ueng-Cheng Yang7,8, Ki Wha Chung12, Byung-Ok Choi13, Garth A Nicholson14, Marina L Kennerson14, Chih-Chiang Chan15,16, Peter De Jonghe5,6,17, Tzu-Hao Cheng3,9, Yi-Chu Liao1,2, Stephan Züchner18, Jonathan Baets5,6,17, Yi-Chung Lee1,2,3.
Abstract
Distal hereditary motor neuropathy is a heterogeneous group of inherited neuropathies characterized by distal limb muscle weakness and atrophy. Although at least 15 genes have been implicated in distal hereditary motor neuropathy, the genetic causes remain elusive in many families. To identify an additional causal gene for distal hereditary motor neuropathy, we performed exome sequencing for two affected individuals and two unaffected members in a Taiwanese family with an autosomal dominant distal hereditary motor neuropathy in which mutations in common distal hereditary motor neuropathy-implicated genes had been excluded. The exome sequencing revealed a heterozygous mutation, c.770A > G (p.His257Arg), in the cytoplasmic tryptophanyl-tRNA synthetase (TrpRS) gene (WARS) that co-segregates with the neuropathy in the family. Further analyses of WARS in an additional 79 Taiwanese pedigrees with inherited neuropathies and 163 index cases from Australian, European, and Korean distal hereditary motor neuropathy families identified the same mutation in another Taiwanese distal hereditary motor neuropathy pedigree with different ancestries and one additional Belgian distal hereditary motor neuropathy family of Caucasian origin. Cell transfection studies demonstrated a dominant-negative effect of the p.His257Arg mutation on aminoacylation activity of TrpRS, which subsequently compromised protein synthesis and reduced cell viability. His257Arg TrpRS also inhibited neurite outgrowth and led to neurite degeneration in the neuronal cell lines and rat motor neurons. Further in vitro analyses showed that the WARS mutation could potentiate the angiostatic activities of TrpRS by enhancing its interaction with vascular endothelial-cadherin. Taken together, these findings establish WARS as a gene whose mutations may cause distal hereditary motor neuropathy and alter canonical and non-canonical functions of TrpRS.Entities:
Keywords: WARS; dHMN; distal hereditary motor neuropathy; exome sequencing; tryptophanyl-tRNA synthetase
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Year: 2017 PMID: 28369220 PMCID: PMC6248622 DOI: 10.1093/brain/awx058
Source DB: PubMed Journal: Brain ISSN: 0006-8950 Impact factor: 13.501