Novel promoter and splice junction defects add to the genetic, clinical or geographic heterogeneity of beta-thalassaemia in the Portuguese population

Hum Genet. 1992 Jul;89(5):573-6. doi: 10.1007/BF00219188.

Abstract

In order to delineate the spectrum and the relative abundance of beta-globin gene defects causing thalassaemia in the Portuguese population, a representative sample was analysed including 51 beta-thalassaemia carriers along with 26 patients representing different clinical phenotypes. Seven mutations were identified, four of which [codon 39 (C----T), 39%; intervening sequence (IVS) 1 nucleotide (nt) 1 (G----A), 26%; IVS 1 nt 110 (G----A), 17%; IVS 1 nt 6 (T----C), 15%] account for 97% of 93 beta-thalassaemia chromosomes. Two previously undescribed mutations, namely a C----T substitution at position--90 in the proximal CACCC box, and the deletion of nucleotides 4 and 5 (AG) in IVS2 were identified. The uncommon, though ubiquitous, G----T transversion at codon 121 was found once upon haplotype V. Direct prenatal diagnosis can be offered to 95% of couples at risk of bearing a thalassaemic child.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chromosome Aberrations / genetics*
  • Chromosome Inversion
  • Codon / genetics
  • Exons / genetics
  • Female
  • Genetic Variation*
  • Genotype
  • Globins / genetics
  • Haplotypes
  • Humans
  • Introns / genetics
  • Mutation
  • Portugal / epidemiology
  • Promoter Regions, Genetic / genetics
  • RNA Splicing
  • Thalassemia / epidemiology
  • Thalassemia / genetics*

Substances

  • Codon
  • Globins