The intron 7 donor splice site transition: a second Tay-Sachs disease mutation in French Canada
✍ Scribed by Peter Hechtman; Bernard Boulay; Marc Braekeleer; Eve Andermann; Serge Melançon; Jean Larochelle; Claude Prevost; Feige Kaplan
- Book ID
- 104669509
- Publisher
- Springer
- Year
- 1992
- Tongue
- English
- Weight
- 715 KB
- Volume
- 90
- Category
- Article
- ISSN
- 0340-6717
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✦ Synopsis
Mutations at the hexosaminidase A (HEXA) gene which cause Tay-Sachs disease (TSD) have elevated frequency in the Ashkenazi Jewish and French-Canadian populations. We report a novel TSD allele in the French-Canadian population associated with the infantile form of the disease. The mutation, a G-->A transition at the +1 position of intron 7, abolishes the donor splice site. Cultured human fibroblasts from a compound heterozygote for this transition (and for a deletion mutation) produce no detectable HEXA mRNA. The intron 7 + 1 mutation occurs in the base adjacent to the site of the adult-onset TSD mutation (G805A). In both mutations a restriction site for the endonuclease EcoRII is abolished. Unambiguous diagnosis, therefore, requires allele-specific oligonucleotide hybridization to distinguish between these two mutant alleles. The intron 7 + 1 mutation has been detected in three unrelated families. Obligate heterozygotes for the intron 7 + 1 mutation were born in the Saguenay-Lac-St-Jean region of Quebec. The most recent ancestors common to obligate carriers of this mutation were from the Charlevoix region of the province of Quebec. This mutation thus has a different geographic centre of diffusion and is probably less common than the exon 1 deletion TSD mutation in French Canadians. Neither mutation has been detected in France, the ancestral homeland of French Canada.
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