A novel intronic variant in UBE3A identified by genome sequencing in a patient with an atypical presentation of Angelman syndrome

Am J Med Genet A. 2020 Sep;182(9):2145-2151. doi: 10.1002/ajmg.a.61740. Epub 2020 Jul 11.

Abstract

Angelman syndrome (AS) is a genetic neurodevelopmental disorder caused by loss or deficient expression of UBE3A on the maternally inherited allele. In 10-15% of individuals with a clinical diagnosis of AS, a molecular diagnosis cannot be established with conventional testing. We describe a 13-year-old male with an atypical presentation of AS, who was found to have a novel, maternally inherited, intronic variant in UBE3A (c.3-12T>A) using genome sequencing (GS). Targeted sequencing of RNA isolated from blood confirmed the creation of a new acceptor splice site. These GS results ended a six-year diagnostic odyssey and revealed a 50% recurrence risk for the unaffected parents. This case illustrates a previously unreported splicing variant causing AS. Intronic variants identifiable by GS may account for a proportion of individuals who are suspected of having well-known genetic disorders despite negative prior genetic testing.

Keywords: Angelman syndrome; UBE3A; genetic counseling; genome sequencing; intronic.

Publication types

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

MeSH terms

  • Adolescent
  • Alleles
  • Angelman Syndrome / genetics*
  • Angelman Syndrome / pathology
  • Child
  • Chromosome Mapping
  • Genetic Predisposition to Disease*
  • Genetic Variation / genetics
  • Humans
  • Introns / genetics*
  • Male
  • Mutation / genetics
  • RNA Splice Sites / genetics
  • Ubiquitin-Protein Ligases / genetics*
  • Whole Genome Sequencing / methods

Substances

  • RNA Splice Sites
  • UBE3A protein, human
  • Ubiquitin-Protein Ligases

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