| Literature DB >> 28905505 |
Saskia B Wortmann1,2,3, Sharita Timal4,5, Hanka Venselaar6, Liesbeth T Wintjes4, Robert Kopajtich2, René G Feichtinger1, Carla Onnekink7,8, Mareike Mühlmeister4, Ulrich Brandt4, Jan A Smeitink4, Joris A Veltman9,10, Wolfgang Sperl1, Dirk Lefeber5, Ger Pruijn7,8, Vesna Stojanovic11,12, Peter Freisinger13, Francjan V Spronsen14, Terry Gj Derks14, Hermine E Veenstra-Knol15, Johannes A Mayr1, Agnes Rötig16, Mark Tarnopolsky17, Holger Prokisch2,3, Richard J Rodenburg4.
Abstract
Mitochondrial protein synthesis involves an intricate interplay between mitochondrial DNA encoded RNAs and nuclear DNA encoded proteins, such as ribosomal proteins and aminoacyl-tRNA synthases. Eukaryotic cells contain 17 mitochondria-specific aminoacyl-tRNA synthases. WARS2 encodes mitochondrial tryptophanyl-tRNA synthase (mtTrpRS), a homodimeric class Ic enzyme (mitochondrial tryptophan-tRNA ligase; EC 6.1.1.2). Here, we report six individuals from five families presenting with either severe neonatal onset lactic acidosis, encephalomyopathy and early death or a later onset, more attenuated course of disease with predominating intellectual disability. Respiratory chain enzymes were usually normal in muscle and fibroblasts, while a severe combined respiratory chain deficiency was found in the liver of a severely affected individual. Exome sequencing revealed rare biallelic variants in WARS2 in all affected individuals. An increase of uncharged mitochondrial tRNATrp and a decrease of mtTrpRS protein content were found in fibroblasts of affected individuals. We hereby define the clinical, neuroradiological, and metabolic phenotype of WARS2 defects. This confidently implicates that mutations in WARS2 cause mitochondrial disease with a broad spectrum of clinical presentation.Entities:
Keywords: COX deficiency; lactic acidosis; liver; mitochondrial disorder
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Year: 2017 PMID: 28905505 DOI: 10.1002/humu.23340
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878