An A-to-G mutation at the +3 position of intron 8 of the HEXA gene is associated with exon 8 skipping and Tay-Sachs disease

Biochem Mol Med. 1995 Jun;55(1):74-6. doi: 10.1006/bmme.1995.1035.

Abstract

Tay-Sachs disease (TSD) results from a deficiency of beta-hexosaminidase A (EC 3.2.1.52) activity. A child with late-infantile TSD was found to have two HEXA mutations, 986 + 3A-->G (A-->G at the +3 position of intron 8) and 533G-->A, associated with the variant B1 form of TSD. We were able to detect exon 8-deleted, but no correctly spliced HEXA mRNA, from the non-533G-->A allele in this patient. This suggests that 986 + 3A-->G results in missplicing and, together with 533G-->A, TSD.

Publication types

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

MeSH terms

  • Alleles
  • Base Sequence
  • Child
  • DNA Primers / genetics
  • Exons
  • Female
  • Heterozygote
  • Hexosaminidase A
  • Humans
  • Introns
  • Molecular Sequence Data
  • Point Mutation*
  • RNA Splicing / genetics
  • RNA, Messenger / genetics
  • Tay-Sachs Disease / genetics*
  • beta-N-Acetylhexosaminidases / genetics*

Substances

  • DNA Primers
  • RNA, Messenger
  • Hexosaminidase A
  • beta-N-Acetylhexosaminidases