Phenotype-guided whole genome analysis in a patient with genetically elusive long QT syndrome yields a novel TRDN-encoded triadin pathogenetic substrate for triadin knockout syndrome and reveals a novel primate-specific cardiac TRDN transcript.

Background: Triadin knockout syndrome (TKOS) is a rare arrhythmia syndrome caused by recessive null variants in TRDN-encoded cardiac triadin 1. TKOS has presented frequently with cardiac arrest in childhood.Objective: The purpose of this study was to elucidate the underlying genetic mechanism of dis...

Descripción completa

Detalles Bibliográficos
Publicado en:Heart Rhythm Vol. 17; no. 6; pp. 1017 - 1025
Autores principales: Clemens, Daniel J., Tester, David J., Marty, Isabelle, Ackerman, Michael J.
Formato: research tables/charts Journal Article
Publicado: Elsevier B.V. Jun2020
Acceso en línea:Ver este registro en EBSCOhost
fields @attributes:
  recordID: 1
pdfLink:
plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=143310367&site=ehost-live
header:
  @attributes:
    shortDbName: ccm
    uiTerm: 143310367
    longDbName: CINAHL Complete
    uiTag: AN
  controlInfo:
    bkinfo:
    dissinfo:
    jinfo:
      jid:
        15475271
        EHI
      jtl: Heart Rhythm
      issn: 15475271
      maglogo: N
    pubinfo:
      dt: Jun2020
      vid: 17
      iid: 6
      pid: 467
      pub: Elsevier B.V.
      place: New York, New York
    artinfo:
      ui:
        143310367
        143310367
        NLM32402482
        143310367
        10.1016/j.hrthm.2020.01.012
        NLM32402482
        143310367
      ppf: 1017
      ppct: 8
      formats:
      tig:
        atl: Phenotype-guided whole genome analysis in a patient with genetically elusive long QT syndrome yields a novel TRDN-encoded triadin pathogenetic substrate for triadin knockout syndrome and reveals a novel primate-specific cardiac TRDN transcript.
      aug:
        au:
          Clemens, Daniel J.
          Tester, David J.
          Marty, Isabelle
          Ackerman, Michael J.
        affil: Windland Smith Rice Sudden Death Genomics Laboratory, Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota
      sug:
        subj:
          Muscle Proteins
          Carrier Proteins
          Electrocardiography
          Long QT Syndrome
          Male
          Carrier Proteins Metabolism
          Nucleotides
          Phenotype
          Adolescence
          Muscle Proteins Metabolism
          Long QT Syndrome Physiopathology
          Long QT Syndrome Metabolism
          Human
          Comparative Studies
          Multicenter Studies
          Evaluation Research
          Validation Studies
          Short Portable Mental Status Questionnaire
          Questionnaires
          Adolescent: 13-18 years
          Male
      ab: Background: Triadin knockout syndrome (TKOS) is a rare arrhythmia syndrome caused by recessive null variants in TRDN-encoded cardiac triadin 1. TKOS has presented frequently with cardiac arrest in childhood.Objective: The purpose of this study was to elucidate the underlying genetic mechanism of disease in a genetically elusive patient displaying a characteristic TKOS phenotype.Methods: Genome sequencing and a TRDN gene-specific trio analysis were completed on the patient. RNA and protein isolated from patient-specific human-induced pluripotent stem cell-derived cardiomyocytes were used to determine the effects of the identified variants using reverse transcription polymerase chain reaction (RT-PCR) and Western blot.Results: Genome sequencing revealed compound heterozygous putative splice-error variants (maternal c.22+29A>G and paternal c.484+1189G>A). The novel paternally derived c.484+1189G>A variant is located within 24 base pairs of a predicted alternative exon 6 (exon 6a), which resides within the intron between canonical exons 5 and 6. We determined that this previously unrecognized exon 6a produces a short TRDN transcript and potentially a novel protein isoform in the normal human heart. The c.484+1189G>A variant not only results in abnormal splicing of the exon 6a-containing transcript leading to a frameshift mutation but also results in the abolishment of the 8-exon cardiac triadin 1 transcript.Conclusion: Here, we present evidence for a novel alternative exon 6a-containing TRDN transcript in the normal heart. The novel deep intronic TRDN variant identified in a patient with TKOS leads to splicing error of a newly recognized exon 6a and loss of triadin. Considering that both TRDN variants in this patient were missed after commercial testing, these results highlight the importance of using genome sequencing when identifying patients with TKOS.
      pubtype: Academic Journal
      doctype:
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
    refInfo:
    holdings:
      @attributes:
        islocal: N