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Novel pathogenic COX20 variants causing dysarthria, ataxia, and sensory neuropathy
Journal article   Open access   Peer reviewed

Novel pathogenic COX20 variants causing dysarthria, ataxia, and sensory neuropathy

Maria G Otero, Emmanuelle Tiongson, Frank Diaz, Katrina Haude, Karin Panzer, Ashley Collier, Jaemin Kim, David Adams, Cynthia J Tifft, Hong Cui, …
Annals of clinical and translational neurology, Vol.6(1), pp.154-160
01/2019
DOI: 10.1002/acn3.661
PMCID: PMC6331954
PMID: 30656193
url
https://doi.org/10.1002/acn3.661View
Published (Version of record) Open Access

Abstract

COX20/FAM36A encodes a mitochondrial complex IV assembly factor important for COX2 activation. Only one homozygous COX20 missense mutation has been previously described in two separate consanguineous families. We report four subjects with features that include childhood hypotonia, areflexia, ataxia, dysarthria, dystonia, and sensory neuropathy. Exome sequencing in all four subjects identified the same novel COX20 variants. One variant affected the splice donor site of intron-one (c.41A>G), while the other variant (c.157+3G>C) affected the splice donor site of intron-two. cDNA and protein analysis indicated that no full-length cDNA or protein was generated. These subjects expand the phenotype associated with COX20 deficiency.
Phenotype Pedigree Humans Adolescent Adult Female Hereditary Sensory and Autonomic Neuropathies - genetics Male Electron Transport Complex IV - genetics Ataxia - genetics Child Dysarthria - genetics

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