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Erythrocyte glycophorin B deficiency may occur by two distinct gene alterations

The genomic DNA from rare persons whose erythrocytes are deficient in glycophorin B (GPB) (S‐s‐U‐ phenotype), was examined by Southern hybridizations using glycophorin B probes and was subdivided into two main categories. In the type I variant (Fav., M.H., S.K.), we found that the S‐s‐U‐ condition is generated by a large gene deletion extending from exons B2 to B4 of glycophorin B gene. Conversely, in the type II variant (Del.), the entire gene is present, and its promoter is almost similar to common Glycophorin A(GPA) and GPB as well as to type I promoters, except for four‐point mutations, which do not occur in potential cis‐acting elements. We concluded that the same phenotypic glycophorin B deficiency may occur by different gene alterations, including either a gene deletion or a mutation that might alter transcription or translation of the gene.