THE POLYADENYLATION SITE MUTATION IN THE ALPHA-GLOBIN GENE-CLUSTER

  • 1 February 1988
    • journal article
    • research article
    • Vol. 71  (2) , 313-319
Abstract
In a previous study, we described a form of nondeletion .alpha.-thalassemia (.alpha.T Saudi.alpha.) found in subjects of Saudi Arabian origin. In the current study, using synthetic oligoprobe hybridization and restriction enzyme analysis, we have demonstrated that the molecular basis of .alpha.T Saudi.alpha. is due solely to a single base mutation (AATAAA .fwdarw. AATAAG) in the polyadenylation signal of the .alpha.2 gene and that the frameshift mutation in codon 14 of the linked .alpha.1 gene is the result of a cloning artefact. The .alpha.2 polyadenylation signal mutation occurs in other Middle Eastern and the Mediterranean populations and is responsible for the clinical phenotype of Hb H disease in some Saudi Arabian individuals with five .alpha. genes (.alpha.T Saudi.alpha./(.alpha..alpha..alpha.)T Saudi). Evidence suggests that the (.alpha..alpha..alpha.)T Saudi haplotype has arise as a result of a recombination between two misaligned chromosomes bearing the .alpha.T Saudi .alpha. defect.