First submicroscopic inversion of the OPA1 gene identified in dominant optic atrophy - a case report

BMC Med Genet. 2020 Nov 26;21(1):236. doi: 10.1186/s12881-020-01166-z.

Abstract

Background: Dominant optic atrophy (DOA) is an inherited optic neuropathy that mainly affects visual acuity, central visual fields and color vision due to a progressive loss of retinal ganglion cells and their axons that form the optic nerve. Approximately 45-90% of affected individuals with DOA harbor pathogenic variants in the OPA1 gene. The mutation spectrum of OPA1 comprises nonsense, canonical and non-canonical splice site, frameshift and missense as well as copy number variants, but intragenic inversions have not been reported so far.

Case presentation: We report a 33-year-old male with characteristic clinical features of DOA. Whole-genome sequencing identified a structural variant of 2.4 kb comprising an inversion of 937 bp at the OPA1 locus. Fine mapping of the breakpoints to single nucleotide level revealed that the structural variation was an inversion flanked by two deletions. As this rearrangement inverts the entire first exon of OPA1, it was classified as likely pathogenic.

Conclusions: We report the first DOA case harboring an inversion in the OPA1 gene. Our study demonstrates that copy-neutral genomic rearrangements have to be considered as a possible cause of disease in DOA cases.

Keywords: Case report; Complex rearrangement; Dominant optic atrophy; Inversion; Non-homologous end joining (NHEJ); OPA1.

Publication types

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

MeSH terms

  • Adult
  • Axons
  • Base Sequence
  • GTP Phosphohydrolases / deficiency
  • GTP Phosphohydrolases / genetics*
  • Gene Expression
  • Humans
  • Male
  • Optic Atrophy, Autosomal Dominant / diagnosis
  • Optic Atrophy, Autosomal Dominant / genetics*
  • Optic Atrophy, Autosomal Dominant / pathology
  • Sequence Inversion*
  • Tomography, Optical Coherence
  • Whole Genome Sequencing

Substances

  • GTP Phosphohydrolases
  • OPA1 protein, human