A novel compound heterozygous mutation in Werner syndrome results in WRN transcript decay

Br J Dermatol. 2005 May;152(5):1030-2. doi: 10.1111/j.1365-2133.2005.06483.x.

Abstract

Background: Werner syndrome (WS) is a rare autosomal recessive progeroid disorder caused by mutations of the WRN gene encoding a protein of the RecQ-type family of DNA helicases.

Objectives: To develop a rapid and simple reverse transcription-polymerase chain reaction (RT-PCR) strategy for mutation analysis of the WRN gene, to identify pathogenic mutations in a German patient with WS and to determine the effects of the pathogenic mutations on WRN mRNA stability.

Methods: Allele-specific RT-PCR, semiquantitative RT-PCR, DNA sequencing.

Results: We describe a novel and rapid RT-PCR-based method for mutation analysis in WS and report a German patient with WS carrying a previously reported (1396delA) as well as a novel nonsense mutation (2334delAC) of the WRN gene. By semiquantitative RT-PCR analysis we demonstrate that this compound heterozygous genotype leads to WRN transcript decay.

Conclusions: In previous studies WS was primarily attributed to a loss of function of stable truncated WRN gene products. Our findings indicate that mutations can also lead to markedly decreased WRN transcript stability.

Publication types

  • Case Reports

MeSH terms

  • Base Sequence
  • Codon, Nonsense
  • DNA Helicases / genetics*
  • DNA, Complementary / genetics
  • Exodeoxyribonucleases
  • Facies
  • Gene Deletion
  • Heterozygote
  • Humans
  • Male
  • Middle Aged
  • Molecular Sequence Data
  • Mutation*
  • RecQ Helicases
  • Reverse Transcriptase Polymerase Chain Reaction / methods
  • Sequence Analysis, DNA / methods
  • Werner Syndrome / genetics*
  • Werner Syndrome Helicase

Substances

  • Codon, Nonsense
  • DNA, Complementary
  • Exodeoxyribonucleases
  • DNA Helicases
  • RecQ Helicases
  • WRN protein, human
  • Werner Syndrome Helicase