Molecular basis of various forms of maple syrup urine disease in Chilean patients.


Journal

Molecular genetics & genomic medicine
ISSN: 2324-9269
Titre abrégé: Mol Genet Genomic Med
Pays: United States
ID NLM: 101603758

Informations de publication

Date de publication:
05 2021
Historique:
revised: 05 01 2021
received: 10 07 2020
accepted: 13 01 2021
pubmed: 7 5 2021
medline: 20 1 2022
entrez: 6 5 2021
Statut: ppublish

Résumé

Maple syrup urine disease (MSUD) is an autosomal recessive inherited metabolic disorder caused by the deficient activity of the branched-chain α-keto acid dehydrogenase (BCKD) enzymatic complex. BCKD is a mitochondrial complex encoded by four genes: BCKDHA, BCKDHB, DBT, and DLD. MSUD is predominantly caused by mutations in the BCKDHA, BCKDHB, and DBT genes which encode the E1α, E1β, and E2 subunits of the BCKD complex, respectively. The aim of this study was to characterize the genetic basis of MSUD in a cohort of Chilean MSUD patients by identifying point mutations in the BCKDHA, BCKDHB, and DBT genes and to describe their impact on the phenotypic heterogeneity of these patients. This manuscript describes a cross-sectional study of 18 MSUD patients carried out using PCR and DNA sequencing. Four novel pathogenic mutations were identified: one in BCKDHA (p.Thr338Ile), two in BCKDHB (p.Gly336Ser e p.Pro240Thr), and one in DBT (p.Gly406Asp). Four additional pathogenic mutations found in this study have been described previously. There were no correlations between the genotype and phenotype of the patients. If MSUD is diagnosed earlier, with a newborn screening approach, it might be possible to establish genotype-phenotype relationships more efficiently.

Sections du résumé

BACKGROUND
Maple syrup urine disease (MSUD) is an autosomal recessive inherited metabolic disorder caused by the deficient activity of the branched-chain α-keto acid dehydrogenase (BCKD) enzymatic complex. BCKD is a mitochondrial complex encoded by four genes: BCKDHA, BCKDHB, DBT, and DLD. MSUD is predominantly caused by mutations in the BCKDHA, BCKDHB, and DBT genes which encode the E1α, E1β, and E2 subunits of the BCKD complex, respectively. The aim of this study was to characterize the genetic basis of MSUD in a cohort of Chilean MSUD patients by identifying point mutations in the BCKDHA, BCKDHB, and DBT genes and to describe their impact on the phenotypic heterogeneity of these patients.
METHODS
This manuscript describes a cross-sectional study of 18 MSUD patients carried out using PCR and DNA sequencing.
RESULTS
Four novel pathogenic mutations were identified: one in BCKDHA (p.Thr338Ile), two in BCKDHB (p.Gly336Ser e p.Pro240Thr), and one in DBT (p.Gly406Asp). Four additional pathogenic mutations found in this study have been described previously. There were no correlations between the genotype and phenotype of the patients.
CONCLUSION
If MSUD is diagnosed earlier, with a newborn screening approach, it might be possible to establish genotype-phenotype relationships more efficiently.

Identifiants

pubmed: 33955723
doi: 10.1002/mgg3.1616
pmc: PMC8172190
doi:

Substances chimiques

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide) EC 1.2.4.4
Dihydrolipoamide Dehydrogenase EC 1.8.1.4
Acyltransferases EC 2.3.-
dihydrolipoamide acyltransferase EC 2.3.1.-

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1616

Informations de copyright

© 2021 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals LLC.

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Auteurs

Diana Ruffato Resende Campanholi (DRR)

Pediatrics Department, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.

Ana Vitoria Barban Margutti (AVB)

Pediatrics Department, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.

Wilson A Silva (WA)

Genetics Department, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Ribeirão Preto Regional Center of Hematology, National Institute of Science and Technology in Cell Therapy and Cell Therapy Center, Ribeirão Preto, Brazil.
Clinical Hospital Genomic Center, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.

Daniel F Garcia (DF)

Genetics Department, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Ribeirão Preto Regional Center of Hematology, National Institute of Science and Technology in Cell Therapy and Cell Therapy Center, Ribeirão Preto, Brazil.

Greice A Molfetta (GA)

Ribeirão Preto Regional Center of Hematology, National Institute of Science and Technology in Cell Therapy and Cell Therapy Center, Ribeirão Preto, Brazil.
Clinical Hospital Genomic Center, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.

Adriana A Marques (AA)

Ribeirão Preto Regional Center of Hematology, National Institute of Science and Technology in Cell Therapy and Cell Therapy Center, Ribeirão Preto, Brazil.

Ida Vanessa Döederlein Schwartz (IVD)

Genetic Department, Porto Alegre Clinical Hospital, Porto Alegre, Brazil.

V Cornejo (V)

Nutrition and Food Technology Institute, Chile University, Santiago, Chile.

Valerie Hamilton (V)

Nutrition and Food Technology Institute, Chile University, Santiago, Chile.

Gabriela Castro (G)

Nutrition and Food Technology Institute, Chile University, Santiago, Chile.

Fernanda Sperb-Ludwig (F)

Genetic Department, Rio Grande do Sul Federal University, Porto Alegre, Brazil.

Ester S Borges (ES)

School of Medicine, Federal University of São Carlos, São Carlos, Brazil.

José S Camelo (JS)

Pediatrics Department, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.

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Classifications MeSH