A recurrent WARS mutation is a novel cause of autosomal dominant distal hereditary motor neuropathy

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.

[1]  A. Antonellis,et al.  Dimerization is required for GARS-mediated neurotoxicity in dominant CMT disease. , 2016, Human molecular genetics.

[2]  P. Tsai,et al.  Clinical and Molecular Characterization of BSCL2 Mutations in a Taiwanese Cohort with Hereditary Neuropathy , 2016, PloS one.

[3]  James Y. Zou Analysis of protein-coding genetic variation in 60,706 humans , 2015, Nature.

[4]  Xiaowu Gai,et al.  Innovative Genomic Collaboration Using the GENESIS (GEM.app) Platform , 2015, Human mutation.

[5]  R. Burgess,et al.  CMT2D neuropathy is linked to the neomorphic binding activity of glycyl-tRNA synthetase , 2015, Nature.

[6]  A. Ferbert,et al.  Loss of function mutations in HARS cause a spectrum of inherited peripheral neuropathies. , 2015, Brain : a journal of neurology.

[7]  S. Züchner,et al.  Impaired Function is a Common Feature of Neuropathy‐Associated Glycyl‐tRNA Synthetase Mutations , 2014, Human mutation.

[8]  Jana Marie Schwarz,et al.  MutationTaster2: mutation prediction for the deep-sequencing age , 2014, Nature Methods.

[9]  J. Shendure,et al.  A general framework for estimating the relative pathogenicity of human genetic variants , 2014, Nature Genetics.

[10]  J. Polke,et al.  Clinical implications of genetic advances in Charcot–Marie–Tooth disease , 2013, Nature Reviews Neurology.

[11]  A. Antonellis,et al.  To charge or not to charge: mechanistic insights into neuropathy-associated tRNA synthetase mutations. , 2013, Current opinion in genetics & development.

[12]  S. Züchner,et al.  Exome sequencing identifies a significant variant in methionyl-tRNA synthetase (MARS) in a family with late-onset CMT2 , 2013, Journal of Neurology, Neurosurgery & Psychiatry.

[13]  K. Stuart,et al.  A Spectrophotometric Assay for Quantitative Measurement of Aminoacyl-tRNA Synthetase Activity , 2013, Journal of biomolecular screening.

[14]  J. Lupski,et al.  A Loss‐of‐Function Variant in the Human Histidyl‐tRNA Synthetase (HARS) Gene is Neurotoxic In Vivo , 2013, Human mutation.

[15]  Kenny Q. Ye,et al.  An integrated map of genetic variation from 1,092 human genomes , 2012, Nature.

[16]  H. Takashima,et al.  Alanyl-tRNA synthetase mutation in a family with dominant distal hereditary motor neuropathy , 2012, Neurology.

[17]  H. Houlden,et al.  Charcot–Marie–Tooth disease: frequency of genetic subtypes and guidelines for genetic testing , 2012, Journal of Neurology, Neurosurgery & Psychiatry.

[18]  F. Mackenzie,et al.  Diverse roles for VEGF-A in the nervous system , 2012, Development.

[19]  J. Lupski,et al.  A Recurrent loss‐of‐function alanyl‐tRNA synthetase (AARS ) mutation in patients with charcot‐marie‐tooth disease type 2N (CMT2N) , 2012, Human mutation.

[20]  B. Kalmar,et al.  The distal hereditary motor neuropathies , 2011, Journal of Neurology, Neurosurgery & Psychiatry.

[21]  Nancy F. Hansen,et al.  Compound heterozygosity for loss-of-function lysyl-tRNA synthetase mutations in a patient with peripheral neuropathy. , 2010, American journal of human genetics.

[22]  B. Asselbergh,et al.  Mutant HSPB8 causes motor neuron-specific neurite degeneration , 2010, Human molecular genetics.

[23]  E. Broussolle,et al.  A major determinant for binding and aminoacylation of tRNA(Ala) in cytoplasmic Alanyl-tRNA synthetase is mutated in dominant axonal Charcot-Marie-Tooth disease. , 2010, American journal of human genetics.

[24]  W. Robberecht,et al.  Relative contribution of mutations in genes for autosomal dominant distal hereditary motor neuropathies: a genotype-phenotype correlation study. , 2007, Brain : a journal of neurology.

[25]  J. Reader,et al.  Erratum: VE-cadherin links tRNA synthetase cytokine to antiangiogenic function (Journal of Biological Chemistry (2005) 280 (2405-2408)) , 2007 .

[26]  R. Burgess,et al.  An Active Dominant Mutation of Glycyl-tRNA Synthetase Causes Neuropathy in a Charcot-Marie-Tooth 2D Mouse Model , 2006, Neuron.

[27]  Youxin Jin,et al.  Structure of human tryptophanyl-tRNA synthetase in complex with tRNATrp reveals the molecular basis of tRNA recognition and specificity , 2006, Nucleic acids research.

[28]  P. Schimmel,et al.  Two conformations of a crystalline human tRNA synthetase–tRNA complex: implications for protein synthesis , 2006, The EMBO journal.

[29]  M. Ruberg,et al.  The G526R glycyl-tRNA synthetase gene mutation in distal hereditary motor neuropathy type V , 2006, Neurology.

[30]  J. Thevelein,et al.  Disrupted function and axonal distribution of mutant tyrosyl-tRNA synthetase in dominant intermediate Charcot-Marie-Tooth neuropathy , 2006, Nature Genetics.

[31]  K. Jin,et al.  From angiogenesis to neuropathology , 2005, Nature.

[32]  W. Robberecht,et al.  Mutant small heat-shock protein 27 causes axonal Charcot-Marie-Tooth disease and distal hereditary motor neuropathy , 2004, Nature Genetics.

[33]  P. Schimmel,et al.  Relationship of two human tRNA synthetases used in cell signaling. , 2004, Trends in biochemical sciences.

[34]  O. Nureki,et al.  A short peptide insertion crucial for angiostatic activity of human tryptophanyl-tRNA synthetase , 2004, Nature Structural &Molecular Biology.

[35]  K. Fischbeck,et al.  Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V. , 2003, American journal of human genetics.

[36]  P. Schimmel,et al.  A human aminoacyl-tRNA synthetase as a regulator of angiogenesis , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[37]  A. Hinnebusch,et al.  Uncharged tRNA activates GCN2 by displacing the protein kinase moiety from a bipartite tRNA-binding domain. , 2000, Molecular cell.

[38]  M. Delarue Partition of aminoacyl-tRNA synthetases in two different structural classes dating back to early metabolism: Implications for the origin of the genetic code and the nature of protein sequences , 1995, Journal of Molecular Evolution.

[39]  M. Kapoor,et al.  Orthogonal use of a human tRNA synthetase active site to achieve multifunctionality , 2010, Nature Structural &Molecular Biology.

[40]  A. Harding Inherited Neuronal Atrophy and Degeneration Predominantly of Lower Motor Neurons , 2005 .

[41]  D. Söll,et al.  Aminoacyl-tRNA synthesis. , 2000, Annual review of biochemistry.