| Literature DB >> 26553276 |
Ying Yang1,2, Wei Liu3, Zhipeng Fang4, Juan Shi5, Fengyu Che2, Chunxia He1,2, Libo Yao1, Enduo Wang4, Yuanming Wu1,2.
Abstract
Hereditary spastic paraplegia (HSP) is a clinically and genetically heterogeneous group of neurodegenerative disorders characterized by spasticity of the lower limbs due to pyramidal tract dysfunction. Here, we report that a missense homozygous mutation c.424G>T (p.D142Y) in the FARS2 gene, which encodes a mitochondrial phenylalanyl tRNA synthetase (mtPheRS), causes HSP in a Chinese consanguineous family by using combination of homozygous mapping and whole-exome sequencing. Immunohistochemical experiments were performed showing that the FARS2 protein was highly expressed in the Purkinje cells of rat cerebellum. The aminoacylation activity of mtPheRS was severely disrupted by the p.D142Y substitution in vitro not only in the first aminoacylation step but also in the last transfer step. Taken together, our results indicate that a missense mutation in FARS2 contributes to HSP, which has the clinical significance of the regulation of tRNA synthetases in human neurodegenerative diseases.Entities:
Keywords: FARS2; Purkinje cells; hereditary spastic paraplegia; neurodegenerative disorder
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Year: 2015 PMID: 26553276 DOI: 10.1002/humu.22930
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878