The -413C > G substitution in the promoter of the FMR1 gene is not associated with the fragile X syndrome phenotype

Mol Cell Probes. 2010 Apr;24(2):107-9. doi: 10.1016/j.mcp.2009.10.006. Epub 2009 Oct 21.

Abstract

Most common inherited form of intellectual disability, fragile X syndrome is associated to an expansion of greater than 200 CGG repeats in the 5' untranslated region of the FMR1 gene on the X chromosome which causes transcriptional silencing and deficiency of the encoded protein FMRP. Molecular diagnosis is performed through a combination of PCR to identify fewer than 100-150 repeats and of Southern blot analysis to identify longer alleles and the methylation status of the FMR1 promoter. We present a family with one patient with mild mental retardation who showed an atypical profile at Southern analysis due to the -413C > G transversion located in the FMR1 promoter which had been described as possibly associated with mental retardation. We demonstrated this variant in other four family members along three generations, including the maternal grandfather who did not manifest any pathological feature. Though the -413C > G substitution was not found in a large control series, these findings allowed to exclude its role in determining the disease phenotype.

Publication types

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

MeSH terms

  • Aged, 80 and over
  • Base Sequence
  • Child
  • DNA Mutational Analysis
  • Female
  • Fragile X Mental Retardation Protein / genetics*
  • Fragile X Syndrome / genetics*
  • Genetic Predisposition to Disease*
  • Humans
  • Infant, Newborn
  • Male
  • Molecular Sequence Data
  • Pedigree
  • Phenotype
  • Polymorphism, Single Nucleotide / genetics*
  • Pregnancy
  • Promoter Regions, Genetic / genetics*

Substances

  • Fragile X Mental Retardation Protein