Whole-exome sequencing identifies TRIM72 as a candidate gene for autosomal recessive limb-girdle muscular dystrophy

Abstract Background Limb-girdle muscular dystrophies (LGMDs) constitute a genetically diverse group of disorders characterized by progressive proximal muscle weakness and atrophy. Despite advances in genetic diagnostics, numerous cases remain unresolved due to extensive genetic heterogeneity, emphas...

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Main Authors: Abdelaziz Tlili, Abdullah Al Mutery
Format: Article
Language:English
Published: BMC 2025-08-01
Series:Human Genomics
Subjects:
Online Access:https://doi.org/10.1186/s40246-025-00809-7
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author Abdelaziz Tlili
Abdullah Al Mutery
author_facet Abdelaziz Tlili
Abdullah Al Mutery
author_sort Abdelaziz Tlili
collection DOAJ
description Abstract Background Limb-girdle muscular dystrophies (LGMDs) constitute a genetically diverse group of disorders characterized by progressive proximal muscle weakness and atrophy. Despite advances in genetic diagnostics, numerous cases remain unresolved due to extensive genetic heterogeneity, emphasizing the necessity for continued identification of novel pathogenic variants. Results Using whole-exome sequencing (WES) in a Saudi family affected by autosomal recessive LGMD, we identified a novel homozygous frameshift mutation (c.891delT; p.Ala298ArgfsTer64) in the TRIM72 (MG53) gene, which we propose as a strong candidate gene for LGMD. Segregation analysis via Sanger sequencing confirmed that the variant co-segregated precisely with the disease phenotype and was absent in ethnically matched control cohorts. TRIM72 encodes a muscle-specific E3 ubiquitin ligase involved in sarcolemmal membrane repair, critical for maintaining muscle cell integrity. Functional parallels between TRIM72 and the LGMD-associated TRIM32, alongside corroborating evidence from animal models and cellular studies, support the candidacy of TRIM72 in LGMD pathogenesis. Conclusion Our findings identify TRIM72 as a novel candidate gene implicated in autosomal recessive LGMD, expanding the genetic spectrum of this heterogeneous disease. This discovery underscores the critical roles of TRIM family proteins in muscle pathology and reinforces the value of advanced genetic sequencing methodologies in diagnosing unresolved muscular dystrophy cases.
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spelling doaj-art-3b2b6896839f4d3ca3aff20500ba50bd2025-08-20T03:43:20ZengBMCHuman Genomics1479-73642025-08-011911610.1186/s40246-025-00809-7Whole-exome sequencing identifies TRIM72 as a candidate gene for autosomal recessive limb-girdle muscular dystrophyAbdelaziz Tlili0Abdullah Al Mutery1Department of Applied Biology, College of Sciences, University of SharjahDepartment of Applied Biology, College of Sciences, University of SharjahAbstract Background Limb-girdle muscular dystrophies (LGMDs) constitute a genetically diverse group of disorders characterized by progressive proximal muscle weakness and atrophy. Despite advances in genetic diagnostics, numerous cases remain unresolved due to extensive genetic heterogeneity, emphasizing the necessity for continued identification of novel pathogenic variants. Results Using whole-exome sequencing (WES) in a Saudi family affected by autosomal recessive LGMD, we identified a novel homozygous frameshift mutation (c.891delT; p.Ala298ArgfsTer64) in the TRIM72 (MG53) gene, which we propose as a strong candidate gene for LGMD. Segregation analysis via Sanger sequencing confirmed that the variant co-segregated precisely with the disease phenotype and was absent in ethnically matched control cohorts. TRIM72 encodes a muscle-specific E3 ubiquitin ligase involved in sarcolemmal membrane repair, critical for maintaining muscle cell integrity. Functional parallels between TRIM72 and the LGMD-associated TRIM32, alongside corroborating evidence from animal models and cellular studies, support the candidacy of TRIM72 in LGMD pathogenesis. Conclusion Our findings identify TRIM72 as a novel candidate gene implicated in autosomal recessive LGMD, expanding the genetic spectrum of this heterogeneous disease. This discovery underscores the critical roles of TRIM family proteins in muscle pathology and reinforces the value of advanced genetic sequencing methodologies in diagnosing unresolved muscular dystrophy cases.https://doi.org/10.1186/s40246-025-00809-7Limb-girdle muscular dystrophiesAutosomal recessiveTRIM72 geneFrameshift mutation
spellingShingle Abdelaziz Tlili
Abdullah Al Mutery
Whole-exome sequencing identifies TRIM72 as a candidate gene for autosomal recessive limb-girdle muscular dystrophy
Human Genomics
Limb-girdle muscular dystrophies
Autosomal recessive
TRIM72 gene
Frameshift mutation
title Whole-exome sequencing identifies TRIM72 as a candidate gene for autosomal recessive limb-girdle muscular dystrophy
title_full Whole-exome sequencing identifies TRIM72 as a candidate gene for autosomal recessive limb-girdle muscular dystrophy
title_fullStr Whole-exome sequencing identifies TRIM72 as a candidate gene for autosomal recessive limb-girdle muscular dystrophy
title_full_unstemmed Whole-exome sequencing identifies TRIM72 as a candidate gene for autosomal recessive limb-girdle muscular dystrophy
title_short Whole-exome sequencing identifies TRIM72 as a candidate gene for autosomal recessive limb-girdle muscular dystrophy
title_sort whole exome sequencing identifies trim72 as a candidate gene for autosomal recessive limb girdle muscular dystrophy
topic Limb-girdle muscular dystrophies
Autosomal recessive
TRIM72 gene
Frameshift mutation
url https://doi.org/10.1186/s40246-025-00809-7
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AT abdullahalmutery wholeexomesequencingidentifiestrim72asacandidategeneforautosomalrecessivelimbgirdlemusculardystrophy