genetics human genetics molecular biology mutation, missense phenotype

Journal

Journal of medical genetics
ISSN: 1468-6244
Titre abrégé: J Med Genet
Pays: England
ID NLM: 2985087R

Informations de publication

Date de publication:
30 Jun 2023
Historique:
received: 08 03 2023
accepted: 09 06 2023
medline: 3 7 2023
pubmed: 3 7 2023
entrez: 3 7 2023
Statut: aheadofprint

Résumé

Otosclerosis is a common cause of adult-onset progressive hearing loss, affecting 0.3%-0.4% of the population. It results from dysregulation of bone homeostasis in the otic capsule, most commonly leading to fixation of the stapes bone, impairing sound conduction through the middle ear. Otosclerosis has a well-known genetic predisposition including familial cases with apparent autosomal dominant mode of inheritance. While linkage analysis and genome-wide association studies suggested an association with several genomic loci and with genes encoding structural proteins involved in bone formation or metabolism, the molecular genetic pathophysiology of human otosclerosis is yet mostly unknown. Whole-exome sequencing, linkage analysis, generation of CRISPR mutant mice, hearing tests and micro-CT. Through genetic studies of kindred with seven individuals affected by apparent autosomal dominant otosclerosis, we identified a disease-causing variant in We demonstrate that otosclerosis can be caused by a variant in

Sections du résumé

BACKGROUND BACKGROUND
Otosclerosis is a common cause of adult-onset progressive hearing loss, affecting 0.3%-0.4% of the population. It results from dysregulation of bone homeostasis in the otic capsule, most commonly leading to fixation of the stapes bone, impairing sound conduction through the middle ear. Otosclerosis has a well-known genetic predisposition including familial cases with apparent autosomal dominant mode of inheritance. While linkage analysis and genome-wide association studies suggested an association with several genomic loci and with genes encoding structural proteins involved in bone formation or metabolism, the molecular genetic pathophysiology of human otosclerosis is yet mostly unknown.
METHODS METHODS
Whole-exome sequencing, linkage analysis, generation of CRISPR mutant mice, hearing tests and micro-CT.
RESULTS RESULTS
Through genetic studies of kindred with seven individuals affected by apparent autosomal dominant otosclerosis, we identified a disease-causing variant in
CONCLUSION CONCLUSIONS
We demonstrate that otosclerosis can be caused by a variant in

Identifiants

pubmed: 37399313
pii: jmg-2023-109264
doi: 10.1136/jmg-2023-109264
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NIDCD NIH HHS
ID : R01 DC011835
Pays : United States

Informations de copyright

© Author(s) (or their employer(s)) 2023. No commercial re-use. See rights and permissions. Published by BMJ.

Déclaration de conflit d'intérêts

Competing interests: None declared.

Auteurs

Max Drabkin (M)

The Morris Kahn Laboratory of Human Genetics, Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel.

Matan M Jean (MM)

The Morris Kahn Laboratory of Human Genetics, Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel.

Yael Noy (Y)

Department of Human Molecular Genetics and Biochemistry, Faculty of Medicine and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.

Daniel Halperin (D)

The Morris Kahn Laboratory of Human Genetics, Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel.

Yuval Yogev (Y)

The Morris Kahn Laboratory of Human Genetics, Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel.

Ohad Wormser (O)

The Morris Kahn Laboratory of Human Genetics, Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel.

Regina Proskorovski-Ohayon (R)

The Morris Kahn Laboratory of Human Genetics, Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel.

Vadim Dolgin (V)

The Morris Kahn Laboratory of Human Genetics, Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel.

Noam Levaot (N)

Department of Physiology and Cell Biology, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Vlad Brumfeld (V)

Department of Chemical Research Support, Weizmann Institute of Science, Rehovot, Israel.

Shira Ovadia (S)

Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Mor Kishner (M)

Department of Life Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Udi Kazenell (U)

Department of Otolaryngology, Head and Neck Surgery, Kaplan Medical Center, Rehovot, Israel.

Karen B Avraham (KB)

Department of Human Molecular Genetics and Biochemistry, Faculty of Medicine and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.

Ilan Shelef (I)

Department of Radiology, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Ohad S Birk (OS)

The Morris Kahn Laboratory of Human Genetics, Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel obirk@bgu.ac.il.
Genetics Institute, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Classifications MeSH