Infantile onset encephalomyopathy, retinopathy, optic atrophy, and mitochondrial DNA depletion associated with a novel pathogenic DHX16 variant.
Milla-Riikka HautakangasPaula WidgrenPaavo KorpelainenSalla M KangasTuomas KomulainenPäivi VieiraElisa RahikkalaKatri PylkäsHannu TuominenHannaleena KokkonenIlkka MiinalainenJavad NadafJacek MajewskiReetta HinttalaJohanna UusimaaPublished in: Clinical genetics (2023)
We studied a patient with mitochondrial DNA depletion in skeletal muscle and a multiorgan phenotype, including fatal encephalomyopathy, retinopathy, optic atrophy, and sensorineural hearing loss. Instead of pathogenic variants in the mitochondrial maintenance genes, we identified previously unpublished variant in DHX16 gene, a de novo heterozygous c.1360C>T (p. Arg454Trp). Variants in DHX16 encoding for DEAH-box RNA helicase have previously been reported only in five patients with a phenotype called as neuromuscular oculoauditory syndrome including developmental delay, neuromuscular symptoms, and ocular or auditory defects with or without seizures. We performed functional studies on patient-derived fibroblasts and skeletal muscle revealing, that the DHX16 expression was decreased. Clinical features together with functional data suggest, that our patient's disease is associated with a novel pathogenic DHX16 variant, and mtDNA depletion could be a secondary manifestation of the disease.
Keyphrases
- mitochondrial dna
- copy number
- skeletal muscle
- genome wide
- case report
- dna methylation
- insulin resistance
- optic nerve
- optical coherence tomography
- oxidative stress
- transcription factor
- binding protein
- working memory
- type diabetes
- early onset
- gene expression
- machine learning
- physical activity
- hearing loss
- deep learning
- big data
- bioinformatics analysis