A biallelic variant of DCAF13 implicated in a neuromuscular disorder in humans.


Journal

European journal of human genetics : EJHG
ISSN: 1476-5438
Titre abrégé: Eur J Hum Genet
Pays: England
ID NLM: 9302235

Informations de publication

Date de publication:
Jun 2023
Historique:
received: 29 08 2022
accepted: 09 02 2023
revised: 05 02 2023
pmc-release: 01 06 2024
medline: 12 6 2023
pubmed: 17 2 2023
entrez: 16 2 2023
Statut: ppublish

Résumé

Neuromuscular disorders encompass a broad range of phenotypes and genetic causes. We investigated a consanguineous family in which multiple patients had a neuromuscular disorder characterized by a waddling gait, limb deformities, muscular weakness and facial palsy. Exome sequencing was completed on the DNA of three of the four patients. We identified a novel missense variant in DCAF13, ENST00000612750.5, NM_015420.7, c.907 G > A;p.(Asp303Asn), ENST00000616836.4, NM_015420.6, c.1363 G > A:p.(Asp455Asn) (rs1209794872) segregating with this phenotype; being homozygous in all four affected patients and heterozygous in the unaffected individuals. The variant was extremely rare in the public databases (gnomAD allele frequency 0.000007081); was absent from the DNA of 300 ethnically matched controls and affected an amino acid which has been conserved across 1-2 billion years of evolution in eukaryotes. DCAF13 contains three WD40 domains and is hypothesized to have roles in both rRNA processing and in ubiquitination of proteins. Analysis of DCAF13 with the p.(Asp455Asn) variant predicted that the amino acid change is deleterious and affects a β-hairpin turn, within a WD40 domain of the protein which may decrease protein stability. Previously, a heterozygous variant of DCAF13 NM_015420.6, c.20 G > C:p.(Trp7Ser) with or without a heterozygous missense variant in CCN3, was suggested to cause inherited cortical myoclonic tremor with epilepsy. In addition, a heterozygous DCAF13 variant has been associated with autism spectrum disorder. Our study indicates a potential role of biallelic DCAF13 variants in neuromuscular disorders. Screening of additional patients with similar phenotype may broaden the allelic and phenotypic spectrum due to DCAF13 variants.

Identifiants

pubmed: 36797467
doi: 10.1038/s41431-023-01319-7
pii: 10.1038/s41431-023-01319-7
pmc: PMC10250411
doi:

Substances chimiques

DCAF13 protein, human 0
RNA-Binding Proteins 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

629-637

Subventions

Organisme : Higher Education Commision, Pakistan (Pakistani Higher Education Commission)
ID : 2877

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2023. The Author(s), under exclusive licence to European Society of Human Genetics.

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Auteurs

Humera Manzoor (H)

School of Biological Sciences, University of the Punjab, Quaid-e-Azam Campus, Lahore, 54590, Pakistan.
Department of Human Genetics and Molecular Biology, University of Health Sciences, Lahore, Pakistan.

Hafsa Zahid (H)

School of Biological Sciences, University of the Punjab, Quaid-e-Azam Campus, Lahore, 54590, Pakistan.

Christopher A Emerling (CA)

Biology Department, Reedley College, Reedley, CA, 93654, USA.

Kishore R Kumar (KR)

Molecular Medicine Laboratory and Department of Neurology, Concord Repatriation General Hospital, Concord Clinical School Faculty of Medicine and Health, University of Sydney, Sydney, NSW, Australia.
Kinghorn Centre for Clinical Genomics, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.

Hafiz Muhammad Jafar Hussain (HMJ)

School of Biological Sciences, University of the Punjab, Quaid-e-Azam Campus, Lahore, 54590, Pakistan.

Go Hun Seo (GH)

3billion inc, Seoul, South Korea.

Muhammad Wajid (M)

Department of Zoology, University of Okara, Punjab, Pakistan.

Sadaf Naz (S)

School of Biological Sciences, University of the Punjab, Quaid-e-Azam Campus, Lahore, 54590, Pakistan. naz.sbs@pu.edu.pk.

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