| Literature DB >> 31823625 |
Faezeh Jamali1, Hamid Ghaedi1, Abbas Tafakhori2, Elham Alehabib3, Marjan Chapi1, Narsis Daftarian4, Hossein Darvish5, Javad Jamshidi6,7.
Abstract
The TWNK (C10orf2) gene encodes Twinkle, an essential helicase for mtDNA replication. Homozygous mutations in TWNK can lead to mitochondrial DNA depletion syndrome 7 (MTDPS7) that usually manifests as Infantile onset spinocerebellar ataxia (IOSCA). Here, we report a 15-year-old Iranian boy with three main symptoms; ataxia, sensorineural hearing loss and optic nerves atrophy which were accompanied by other symptoms including flexion contracture, dysarthric speech, nystagmus, dystonia and borderline intellectual disability. Whole exome sequencing (WES) revealed a homozygous mutation in his TWNK gene. The mutation was a transversion which replaced a C with A (NM_021830.4 (TWNK):c.874C>A). This nucleotide substitution results in replacing a Threonine with Proline in codon 292 of Twinkle protein (p.Pro292Thr). In silico analyses showed that this amino acid change in Twinkle could be deleterious and disease-causing; therefore, we attribute the symptoms of our patient to this mutation. Our study extended the homozygous mutation spectrum of the TWNK gene that leads to IOSCA.Entities:
Keywords: C10orf2; Hearing loss; Infantile; Iran; Optic neuropathy; Spinocerebellar ataxia
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Year: 2019 PMID: 31823625
Source DB: PubMed Journal: Arch Iran Med ISSN: 1029-2977 Impact factor: 1.354