A novel missense variant in IDH3A causes autosomal recessive retinitis pigmentosa.


Journal

Ophthalmic genetics
ISSN: 1744-5094
Titre abrégé: Ophthalmic Genet
Pays: England
ID NLM: 9436057

Informations de publication

Date de publication:
04 2019
Historique:
pubmed: 24 4 2019
medline: 14 3 2020
entrez: 24 4 2019
Statut: ppublish

Résumé

Inherited retinal degenerations (IRDs) encompass a wide spectrum of genetic ocular diseases characterized by considerable genetic and clinical heterogeneity. Complete ophthalmic examination and next-generation sequencing. We describe a patient with no family history of vision loss, who at the age of 28 years developed visual impairment consistent with a severe form of retinitis pigmentosa. Genetic testing by means of whole exome sequencing identified a homozygous variant in the gene IDH3A. To date, only three papers have reported mutations in IDH3A, in families with early-onset retinal degeneration with or without the presence of macular pseudocoloboma. This study highlights the importance of including this rarely-mutated gene in the molecular diagnostic set-ups for IRDs, and further delineates the phenotypic spectrum elicited by mutations in IDH3A.

Sections du résumé

BACKGROUND
Inherited retinal degenerations (IRDs) encompass a wide spectrum of genetic ocular diseases characterized by considerable genetic and clinical heterogeneity.
METHODS
Complete ophthalmic examination and next-generation sequencing.
RESULTS
We describe a patient with no family history of vision loss, who at the age of 28 years developed visual impairment consistent with a severe form of retinitis pigmentosa. Genetic testing by means of whole exome sequencing identified a homozygous variant in the gene IDH3A. To date, only three papers have reported mutations in IDH3A, in families with early-onset retinal degeneration with or without the presence of macular pseudocoloboma.
CONCLUSION
This study highlights the importance of including this rarely-mutated gene in the molecular diagnostic set-ups for IRDs, and further delineates the phenotypic spectrum elicited by mutations in IDH3A.

Identifiants

pubmed: 31012789
doi: 10.1080/13816810.2019.1605391
doi:

Substances chimiques

IDH3a protein, human EC 1.1.1.41
Isocitrate Dehydrogenase EC 1.1.1.41

Types de publication

Case Reports Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

177-181

Auteurs

Virginie G Peter (VG)

a Department of Computational Biology, Unit of Medical Genetics , University of Lausanne , Lausanne , Switzerland.
b Department of Genetics and Genome Biology , University of Leicester , Leicester , UK.

Konstantinos Nikopoulos (K)

a Department of Computational Biology, Unit of Medical Genetics , University of Lausanne , Lausanne , Switzerland.
c Service of Medical Genetics , Lausanne University Hospital (CHUV) , Lausanne , Switzerland.

Mathieu Quinodoz (M)

a Department of Computational Biology, Unit of Medical Genetics , University of Lausanne , Lausanne , Switzerland.
b Department of Genetics and Genome Biology , University of Leicester , Leicester , UK.

Lotta Granse (L)

d Department of Ophthalmology , University of Lund , Lund , Sweden.

Pietro Farinelli (P)

e Department of Biology , University of Copenhagen , Copenhagen , OE , Denmark.

Andrea Superti-Furga (A)

c Service of Medical Genetics , Lausanne University Hospital (CHUV) , Lausanne , Switzerland.

Sten Andréasson (S)

d Department of Ophthalmology , University of Lund , Lund , Sweden.

Carlo Rivolta (C)

a Department of Computational Biology, Unit of Medical Genetics , University of Lausanne , Lausanne , Switzerland.
b Department of Genetics and Genome Biology , University of Leicester , Leicester , UK.

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Classifications MeSH