Diagnosis of N-acetylglutamate synthase deficiency by use of cultured fibroblasts and avoidance of nonsense-mediated mRNA decay

J Inherit Metab Dis. 2003;26(6):601-5. doi: 10.1023/a:1025912417548.

Abstract

Molecular diagnosis of N-acetylglutamate synthase deficiency (NAGSD) has become possible now that the corresponding gene has been identified. We describe the genetic analysis of a patient with NAGSD using low-level transcripts derived from cultured fibroblasts. One defective allele (c.1306-1307insT) was detected by PCR amplification. However, the transcript from a second mutation (IVS3 - 2A>T), causing aberrant splicing with the generation of a premature termination codon, was not detected until interference of nonsense-mediated mRNA decay was abrogated by the translation inhibitor cycloheximide. We demonstrate that low-level transcripts in cells that do not express significant enzyme activity are a valuable tool for molecular studies of genetic alterations, and suggest routine abrogation of nonsense-mediated mRNA decay using cycloheximide when transcript analysis is performed.

Publication types

  • Case Reports

MeSH terms

  • Acetyltransferases / deficiency*
  • Alleles
  • Amino Acid Metabolism, Inborn Errors / diagnosis*
  • Amino Acid Metabolism, Inborn Errors / enzymology
  • Amino Acid Metabolism, Inborn Errors / genetics*
  • Amino-Acid N-Acetyltransferase
  • Cells, Cultured
  • Codon / genetics
  • Codon, Nonsense / genetics*
  • Cycloheximide
  • DNA, Complementary / genetics
  • Female
  • Fibroblasts / enzymology*
  • Humans
  • Infant, Newborn
  • Protein Synthesis Inhibitors
  • RNA, Messenger / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transcription, Genetic / drug effects
  • Transcription, Genetic / genetics

Substances

  • Codon
  • Codon, Nonsense
  • DNA, Complementary
  • Protein Synthesis Inhibitors
  • RNA, Messenger
  • Cycloheximide
  • Acetyltransferases
  • Amino-Acid N-Acetyltransferase
  • NAGS protein, human