Missense variant in SRCAP with distinct DNA methylation signature associated with non-FLHS SRCAP-related neurodevelopmental disorder.

SNF2-related CREBBP activator protein gene episignature exome sequencing methylation non-Floating Harbor syndrome SRCAP-related neurodevelopmental disorder

Journal

American journal of medical genetics. Part A
ISSN: 1552-4833
Titre abrégé: Am J Med Genet A
Pays: United States
ID NLM: 101235741

Informations de publication

Date de publication:
10 2023
Historique:
revised: 18 05 2023
received: 17 02 2023
accepted: 26 05 2023
medline: 21 9 2023
pubmed: 21 6 2023
entrez: 21 6 2023
Statut: ppublish

Résumé

Floating-Harbor syndrome (FLHS) is a neurodevelopmental disorder (NDD) caused by truncating variants in exons 33 and 34 of the SNF2-related CREBBP activator protein gene (SRCAP). Truncating variants proximal to this location in SRCAP result in a non-FLHS SRCAP-associated NDD; an overlapping but distinct NDD characterized by developmental delay with or without intellectual disability (ID), hypotonia, normal stature, and behavioral and psychiatric issues. Here, we report a young woman who initially presented in childhood with significant delays in speech and mild ID. In young adulthood, she developed schizophrenia. On physical examination, she had facial features suggestive of 22q11 deletion syndrome. After non-diagnostic chromosomal microarray and trio exome sequencing (ES), a re-analysis of trio ES data identified a de novo missense variant in SRCAP that was proximal to the FLHS critical region. Subsequent DNA methylation studies showed the unique methylation signature associated with pathogenic sequence variants in non-FLHS SRCAP-related NDD. This clinical report describes an individual with non-FLHS SRCAP-related NDD caused by an SRCAP missense variant, and it also demonstrates the clinical utility of ES re-analysis and DNA methylation analysis for undiagnosed patients, in particular, those with variants of uncertain significance.

Identifiants

pubmed: 37340855
doi: 10.1002/ajmg.a.63329
doi:

Substances chimiques

Adenosine Triphosphatases EC 3.6.1.-
SRCAP protein, human EC 3.6.4.-

Types de publication

Case Reports Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2640-2646

Subventions

Organisme : CIHR
Pays : Canada

Informations de copyright

© 2023 Wiley Periodicals LLC.

Références

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Auteurs

Alexandre White-Brown (A)

Children's Hospital of Eastern Ontario Research Institute, University of Ottawa, Ottawa, Ontario, Canada.

Sanaa Choufani (S)

Genetics and Genome Biology Program, Research Institute, The Hospital for Sick Children, Toronto, Ontario, Canada.
Children's Hospital of Eastern Ontario Research Institute, University of Ottawa, Ottawa, Ontario, Canada.

Rosanna Weksberg (R)

Genetics and Genome Biology Program, Research Institute, The Hospital for Sick Children, Toronto, Ontario, Canada.
Division of Clinical and Metabolic Genetics, The Hospital for Sick Children, Toronto, Ontario, Canada.

David Dyment (D)

Children's Hospital of Eastern Ontario Research Institute, University of Ottawa, Ottawa, Ontario, Canada.
Department of Genetics, Children's Hospital of Eastern Ontario, Ottawa, Ontario, Canada.

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