Null mutations and lethal congenital form of glycogen storage disease type IV

Biochem Biophys Res Commun. 2007 Sep 21;361(2):445-50. doi: 10.1016/j.bbrc.2007.07.074. Epub 2007 Jul 24.

Abstract

Glycogen branching enzyme deficiency (glycogen storage disease type IV, GSD-IV) is a rare autosomal recessive disorder of the glycogen synthesis with high mortality. Two female newborns showed severe hypotonia at birth and both died of cardiorespiratory failure, at 4 and 12 weeks, respectively. In both patients, muscle biopsies showed deposits of PAS-positive diastase-resistant material and biochemical analysis in cultured fibroblasts showed markedly reduced glycogen branching enzyme activity. Direct sequencing of GBE1 gene revealed that patient 1 was homozygous for a novel c.691+5 g>c in intron 5 (IVS5+5 g>c). RT-PCR analysis of GBE1 transcripts from fibroblasts cDNA showed that this mutation produce aberrant splicing. Patient 2 was homozygous for a novel c.1643G>A mutation leading to a stop at codon 548 in exon 13 (p.W548X). These data underscore that in GSD-IV a severe phenotype correlates with null mutations, and indicate that RNA analysis is necessary to characterize functional consequences of intronic mutations.

Publication types

  • Case Reports

MeSH terms

  • 1,4-alpha-Glucan Branching Enzyme / chemistry
  • 1,4-alpha-Glucan Branching Enzyme / genetics
  • Amino Acid Sequence
  • Base Sequence
  • Biopsy
  • Blotting, Western
  • DNA Mutational Analysis
  • DNA, Complementary
  • Exons / genetics
  • Fatal Outcome
  • Female
  • Fibroblasts / enzymology
  • Glycogen Storage Disease Type IV / genetics*
  • Humans
  • Infant, Newborn
  • Introns / genetics
  • Molecular Sequence Data
  • Muscle, Skeletal / enzymology
  • Muscle, Skeletal / pathology
  • Mutation / genetics*

Substances

  • DNA, Complementary
  • 1,4-alpha-Glucan Branching Enzyme