A homozygous missense mutation in NEUROD1 is associated with nonsyndromic autosomal recessive retinitis pigmentosa

Invest Ophthalmol Vis Sci. 2014 Dec 4;56(1):150-5. doi: 10.1167/iovs.14-15382.

Abstract

Purpose: Mutations in the same gene can lead to different clinical phenotypes. In this study, we aim to identify novel genotype-phenotype correlations and novel disease genes by analyzing an unsolved autosomal recessive retinitis pigmentosa (ARRP) Han Chinese family.

Methods: Whole exome sequencing was performed for one proband from the consanguineous ARRP family. Stringent variants filtering and prioritizations were applied to identify the causative mutation.

Results: A homozygous missense variant, c.724G>A; p.V242I, in NEUROD1 was identified as the most likely cause of disease. This allele perfectly segregates in the family and affects an amino acid, which is highly conserved among mammals. A previous study showed that a homozygous null allele in NEUROD1 causes severe syndromic disease with neonatal diabetes, systematic neurological abnormalities, and early-onset retinal dystrophy. Consistent with these results, our patients who are homozygous for a less severe missense allele presented only late-onset retinal degeneration without any syndromic symptoms.

Conclusions: We identified a potential novel genotype-phenotype correlation between NEUROD1 and nonsyndromic ARRP. Our study supports the idea that NEUROD1 is important for maintenance of the retina function and partial loss-of-function mutation in NEUROD1 is likely a rare cause of nonsyndromic ARRP.

Keywords: NEUROD1; genotype–phenotype correlation; next-generation sequencing; retina; retinitis pigmentosa.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adult
  • Basic Helix-Loop-Helix Transcription Factors / genetics*
  • Basic Helix-Loop-Helix Transcription Factors / metabolism
  • DNA / genetics*
  • DNA Mutational Analysis
  • Female
  • Genes, Recessive
  • Homozygote
  • Humans
  • Male
  • Mutation, Missense*
  • Pedigree
  • Phenotype
  • Retinitis Pigmentosa / genetics*
  • Retinitis Pigmentosa / metabolism

Substances

  • Basic Helix-Loop-Helix Transcription Factors
  • NEUROD1 protein, human
  • DNA