New clinical and molecular evidence linking mutations in ARSG to Usher syndrome type IV.


Journal

Human mutation
ISSN: 1098-1004
Titre abrégé: Hum Mutat
Pays: United States
ID NLM: 9215429

Informations de publication

Date de publication:
03 2021
Historique:
received: 17 07 2020
revised: 11 11 2020
accepted: 06 12 2020
pubmed: 11 12 2020
medline: 1 4 2022
entrez: 10 12 2020
Statut: ppublish

Résumé

In murine and canine animal models, mutations in the Arylsulfatase G gene (ARSG) cause a particular lysosomal storage disorder characterized by neurological phenotypes. Recently, two variants in the same gene were found to be associated with an atypical form of Usher syndrome in humans, leading to visual and auditory impairment without the involvement of the central nervous system. In this study, we identified three novel pathogenic variants in ARSG, which segregated recessively with the disease in two families from Portugal. The probands were affected with retinitis pigmentosa and sensorineural hearing loss, generally with an onset of symptoms in their fourth decade of life. Functional experiments showed that these pathogenic variants abolish the sulfatase activity of the Arylsulfatase G enzyme and impede the appropriate lysosomal localization of the protein product, which appears to be retained in the endoplasmic reticulum. Our data enable to definitely confirm that different biallelic variants in ARSG cause a specific deaf-blindness syndrome, by abolishing the activity of the enzyme it encodes.

Identifiants

pubmed: 33300174
doi: 10.1002/humu.24150
doi:

Substances chimiques

ARSG protein, human EC 3.1.6.-
Arylsulfatases EC 3.1.6.1

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

261-271

Commentaires et corrections

Type : ErratumIn

Informations de copyright

© 2020 Wiley Periodicals LLC.

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Auteurs

Virginie G Peter (VG)

Institute of Molecular and Clinical Ophthalmology Basel (IOB), Basel, Switzerland.
Department of Ophthalmology, University of Basel, Basel, Switzerland.
Institute of Experimental Pathology, Lausanne University Hospital (CHUV), Lausanne, Switzerland.

Mathieu Quinodoz (M)

Institute of Molecular and Clinical Ophthalmology Basel (IOB), Basel, Switzerland.
Department of Ophthalmology, University of Basel, Basel, Switzerland.
Department of Genetics and Genome Biology, University of Leicester, Leicester, UK.

Silvia Sadio (S)

Department of Ophthalmology, Instituto de Oftalmologia Dr. Gama Pinto, Lisbon, Portugal.

Sebastian Held (S)

Department of Biochemistry, University of Kiel, Kiel, Germany.

Márcia Rodrigues (M)

Department of Medical Genetics, Hospital Santa Maria, Centro Hospitalar Universitário Lisboa Norte (CHULN), Lisbon Academic Medical Center (CAML), Lisbon, Portugal.

Marta Soares (M)

Department of Medical Genetics, Hospital Santa Maria, Centro Hospitalar Universitário Lisboa Norte (CHULN), Lisbon Academic Medical Center (CAML), Lisbon, Portugal.

Ana Berta Sousa (AB)

Department of Medical Genetics, Hospital Santa Maria, Centro Hospitalar Universitário Lisboa Norte (CHULN), Lisbon Academic Medical Center (CAML), Lisbon, Portugal.
Department of Basic Immunology, Medical Faculty, University of Lisbon, Lisbon, Portugal.

Luisa Coutinho Santos (L)

Department of Ophthalmology, Instituto de Oftalmologia Dr. Gama Pinto, Lisbon, Portugal.

Markus Damme (M)

Department of Biochemistry, University of Kiel, Kiel, Germany.

Carlo Rivolta (C)

Institute of Molecular and Clinical Ophthalmology Basel (IOB), Basel, Switzerland.
Department of Ophthalmology, University of Basel, Basel, Switzerland.
Department of Genetics and Genome Biology, University of Leicester, Leicester, UK.

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