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Autosomal dominant in cis D4Z4 repeat array duplication alleles in facioscapulohumeral dystrophy.
Lemmers, Richard J L F; Butterfield, Russell; van der Vliet, Patrick J; de Bleecker, Jan L; van der Pol, Ludo; Dunn, Diane M; Erasmus, Corrie E; D'Hooghe, Marc; Verhoeven, Kristof; Balog, Judit; Bigot, Anne; van Engelen, Baziel; Statland, Jeffrey; Bugiardini, Enrico; van der Stoep, Nienke; Evangelista, Teresinha; Marini-Bettolo, Chiara; van den Bergh, Peter; Tawil, Rabi; Voermans, Nicol C; Vissing, John; Weiss, Robert B; van der Maarel, Silvère M.
Afiliação
  • Lemmers RJLF; Department of Human Genetics, Leiden University Medical Center, 2300 RC, Leiden, The Netherlands.
  • Butterfield R; Department of Pediatrics, University of Utah, Salt Lake City, UT 84112, USA.
  • van der Vliet PJ; Department of Human Genetics, Leiden University Medical Center, 2300 RC, Leiden, The Netherlands.
  • de Bleecker JL; Department of Neurology, University Hospital, 9000 Gent, Belgium.
  • van der Pol L; University Medical Center Utrecht, 3584 EA, Utrecht, The Netherlands.
  • Dunn DM; Department of Human Genetics, University of Utah, Salt Lake City, UT 84112, USA.
  • Erasmus CE; Neuromuscular Centre Nijmegen, Radboud University Nijmegen Medical Centre, 6525 GA, Nijmegen, The Netherlands.
  • D'Hooghe M; Department of Neurology, Algemeen Ziekenhuis Sint-Jan, 8000, Brugge, Belgium.
  • Verhoeven K; Department of Neurology, Algemeen Ziekenhuis Sint-Jan, 8000, Brugge, Belgium.
  • Balog J; Department of Human Genetics, Leiden University Medical Center, 2300 RC, Leiden, The Netherlands.
  • Bigot A; Sorbonne Université, Inserm UMRS974, Institut de Myologie, Centre de Recherche en Myologie, F-75013 Paris, France.
  • van Engelen B; Neuromuscular Centre Nijmegen, Radboud University Nijmegen Medical Centre, 6525 GA, Nijmegen, The Netherlands.
  • Statland J; University of Kansas Medical Center, Kansas City, KS 66103, USA.
  • Bugiardini E; National Hospital For Neurology and Neurosurgery, UCL Queen Square Institute of Neurology, London, WC1N 3BG, UK.
  • van der Stoep N; Department of Clinical Genetics, Leiden University Medical Center, 2300 RC, Leiden, The Netherlands.
  • Evangelista T; Unité de Morphologie Neuromusculaire, Institut de Myologie, AP-HP, F-75013, Paris, France.
  • Marini-Bettolo C; The John Walton Muscular Dystrophy Research Centre, Faculty of Medical Sciences, Newcastle upon Tyne, NE1 3BZ, UK.
  • van den Bergh P; Department of Neurology, Saint-Luc UCL, 1200, Brussels, Belgium.
  • Tawil R; Department of Neurology, University of Rochester Medical Center, NY 14642, Rochester, USA.
  • Voermans NC; Neuromuscular Centre Nijmegen, Radboud University Nijmegen Medical Centre, 6525 GA, Nijmegen, The Netherlands.
  • Vissing J; Department of Neurology, University of Copenhagen, DK-2100 Copenhagen, Denmark.
  • Weiss RB; Department of Human Genetics, University of Utah, Salt Lake City, UT 84112, USA.
  • van der Maarel SM; Department of Human Genetics, Leiden University Medical Center, 2300 RC, Leiden, The Netherlands.
Brain ; 147(2): 414-426, 2024 02 01.
Article em En | MEDLINE | ID: mdl-37703328
Facioscapulohumeral dystrophy (FSHD) has a unique genetic aetiology resulting in partial chromatin relaxation of the D4Z4 macrosatellite repeat array on 4qter. This D4Z4 chromatin relaxation facilitates inappropriate expression of the transcription factor DUX4 in skeletal muscle. DUX4 is encoded by a retrogene that is embedded within the distal region of the D4Z4 repeat array. In the European population, the D4Z4 repeat array is usually organized in a single array that ranges between 8 and 100 units. D4Z4 chromatin relaxation and DUX4 derepression in FSHD is most often caused by repeat array contraction to 1-10 units (FSHD1) or by a digenic mechanism requiring pathogenic variants in a D4Z4 chromatin repressor like SMCHD1, combined with a repeat array between 8 and 20 units (FSHD2). With a prevalence of 1.5% in the European population, in cis duplications of the D4Z4 repeat array, where two adjacent D4Z4 arrays are interrupted by a spacer sequence, are relatively common but their relationship to FSHD is not well understood. In cis duplication alleles were shown to be pathogenic in FSHD2 patients; however, there is inconsistent evidence for the necessity of an SMCHD1 mutation for disease development. To explore the pathogenic nature of these alleles we compared in cis duplication alleles in FSHD patients with or without pathogenic SMCHD1 variant. For both groups we showed duplication-allele-specific DUX4 expression. We studied these alleles in detail using pulsed-field gel electrophoresis-based Southern blotting and molecular combing, emphasizing the challenges in the characterization of these rearrangements. Nanopore sequencing was instrumental to study the composition and methylation of the duplicated D4Z4 repeat arrays and to identify the breakpoints and the spacer sequence between the arrays. By comparing the composition of the D4Z4 repeat array of in cis duplication alleles in both groups, we found that specific combinations of proximal and distal repeat array sizes determine their pathogenicity. Supported by our algorithm to predict pathogenicity, diagnostic laboratories should now be furnished to accurately interpret these in cis D4Z4 repeat array duplications, alleles that can easily be missed in routine settings.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Distrofia Muscular Facioescapuloumeral Tipo de estudo: Prognostic_studies / Risk_factors_studies Limite: Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Distrofia Muscular Facioescapuloumeral Tipo de estudo: Prognostic_studies / Risk_factors_studies Limite: Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article