Linkage analysis of nondeletion hereditary persistence of fetal hemoglobin.
Nondeletion forms of hereditary persistence of fetal hemoglobin may result from regulatory disorders of globin gene expression. The defects in two such conditions were localized by demonstrating a tight genetic linkage between the disorders and polymorphic restriction endonuclease sites within the beta-like globin gene complex. In one instance, the defect probably occurred outside the region of DNA between the epsilon- and beta-globin genes.
D002872:Chromosome Deletion; D004262:DNA Restriction Enzymes; D005260:Female; D005319:Fetal Hemoglobin / Q000235:genetics*; D008040:Genetic Linkage; D005914:Globins / Q000235:genetics; D006801:Humans; D008297:Male; D010375:Pedigree; D011110:Polymorphism, Genetic; D013789:Thalassemia / Q000235:genetics*
D005914:Globins; D005319:Fetal Hemoglobin; D004262:DNA Restriction Enzymes