Whole-exome sequencing in patients with protein aggregate myopathies reveals causative mutations associated with novel atypical phenotypes.


Journal

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
ISSN: 1590-3478
Titre abrégé: Neurol Sci
Pays: Italy
ID NLM: 100959175

Informations de publication

Date de publication:
Jul 2021
Historique:
received: 04 05 2020
accepted: 01 11 2020
pubmed: 11 11 2020
medline: 10 7 2021
entrez: 10 11 2020
Statut: ppublish

Résumé

Myofibrillar myopathies (MFM) are a subgroup of protein aggregate myopathies (PAM) characterized by a common histological picture of myofibrillar dissolution, Z-disk disintegration, and accumulation of degradation products into inclusions. Mutations in genes encoding components of the Z-disk or Z-disk-associated proteins occur in some patients whereas in most of the cases, the causative gene defect is still unknown. We aimed to search for pathogenic mutations in genes not previously associated with MFM phenotype. We performed whole-exome sequencing in four patients from three unrelated families who were diagnosed with PAM without aberrations in causative genes for MFM. In the first patient and her affected daughter, we identified a heterozygous p.(Arg89Cys) missense mutation in LMNA gene which has not been linked with PAM pathology before. In the second patient, a heterozygous p.(Asn4807Phe) mutation in RYR1 not previously described in PAM represents a novel, candidate gene with a possible causative role in the disease. Finally, in the third patient and his symptomatic daughter, we found a previously reported heterozygous p.(Cys30071Arg) mutation in TTN gene that was clinically associated with cardiac involvement. Our study identifies a new genetic background in PAM pathology and expands the clinical phenotype of known pathogenic mutations.

Sections du résumé

BACKGROUND BACKGROUND
Myofibrillar myopathies (MFM) are a subgroup of protein aggregate myopathies (PAM) characterized by a common histological picture of myofibrillar dissolution, Z-disk disintegration, and accumulation of degradation products into inclusions. Mutations in genes encoding components of the Z-disk or Z-disk-associated proteins occur in some patients whereas in most of the cases, the causative gene defect is still unknown. We aimed to search for pathogenic mutations in genes not previously associated with MFM phenotype.
METHODS METHODS
We performed whole-exome sequencing in four patients from three unrelated families who were diagnosed with PAM without aberrations in causative genes for MFM.
RESULTS RESULTS
In the first patient and her affected daughter, we identified a heterozygous p.(Arg89Cys) missense mutation in LMNA gene which has not been linked with PAM pathology before. In the second patient, a heterozygous p.(Asn4807Phe) mutation in RYR1 not previously described in PAM represents a novel, candidate gene with a possible causative role in the disease. Finally, in the third patient and his symptomatic daughter, we found a previously reported heterozygous p.(Cys30071Arg) mutation in TTN gene that was clinically associated with cardiac involvement.
CONCLUSIONS CONCLUSIONS
Our study identifies a new genetic background in PAM pathology and expands the clinical phenotype of known pathogenic mutations.

Identifiants

pubmed: 33170376
doi: 10.1007/s10072-020-04876-7
pii: 10.1007/s10072-020-04876-7
pmc: PMC7654353
doi:

Substances chimiques

Protein Aggregates 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2819-2827

Subventions

Organisme : UE
ID : FP7-REGPOT-2012-CT2012-316254-BASTION

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Auteurs

Marcin M Machnicki (MM)

Department of Immunology, Medical University of Warsaw, Warsaw, Poland.

Valeria Guglielmi (V)

Department of Neurosciences, Biomedicine and Movement Sciences, Section of Clinical Neurology, University of Verona, Verona, Italy.

Elia Pancheri (E)

Department of Neurosciences, Biomedicine and Movement Sciences, Section of Clinical Neurology, University of Verona, Verona, Italy.

Francesca Gualandi (F)

UOL of Medical Genetics, Department of Medical Science, University of Ferrara, Ferrara, Italy.

Lorenzo Verriello (L)

Neurologic Clinic, Department of Neurological Sciences, Azienda Sanitaria Universitaria Integrata di Udine, Udine, Italy.

Katarzyna Pruszczyk (K)

Department of Immunology, Medical University of Warsaw, Warsaw, Poland.

Joanna Kosinska (J)

Department of Medical Genetics, Medical University of Warsaw, Warsaw, Poland.

Antonella Sangalli (A)

Department of Neurosciences, Biomedicine and Movement Sciences, Section of Biology and Genetics, University of Verona, Verona, Italy.

Malgorzata Rydzanicz (M)

Department of Medical Genetics, Medical University of Warsaw, Warsaw, Poland.

Maria Grazia Romanelli (MG)

Department of Neurosciences, Biomedicine and Movement Sciences, Section of Biology and Genetics, University of Verona, Verona, Italy.

Marcella Neri (M)

UOL of Medical Genetics, Department of Medical Science, University of Ferrara, Ferrara, Italy.

Rafal Ploski (R)

Department of Medical Genetics, Medical University of Warsaw, Warsaw, Poland.

Paola Tonin (P)

Department of Neurosciences, Biomedicine and Movement Sciences, Section of Clinical Neurology, University of Verona, Verona, Italy.

Giuliano Tomelleri (G)

Department of Neurosciences, Biomedicine and Movement Sciences, Section of Clinical Neurology, University of Verona, Verona, Italy.

Tomasz Stoklosa (T)

Department of Immunology, Medical University of Warsaw, Warsaw, Poland. tomasz.stoklosa@wum.edu.pl.

Gaetano Vattemi (G)

Department of Neurosciences, Biomedicine and Movement Sciences, Section of Clinical Neurology, University of Verona, Verona, Italy. gaetano.vattemi@univr.it.

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