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Blood group B gene is barely expressed in in vitro erythroid culture of B m ‐derived CD34 + cells without an erythroid cell‐specific regulatory element
Author(s) -
Sano R.,
Nogawa M.,
Nakajima T.,
Takahashi Y.,
Takahashi K.,
Kubo R.,
Kominato Y.,
Yokohama A.,
Tsukada J.,
Yamao H.,
Kishida T.,
Ogasawara K.,
Uchikawa M.
Publication year - 2015
Publication title -
vox sanguinis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.68
H-Index - 83
eISSN - 1423-0410
pISSN - 0042-9007
DOI - 10.1111/vox.12220
Subject(s) - microbiology and biotechnology , biology , cd34 , gata2 , in vitro , abo blood group system , cellular differentiation , gene , haematopoiesis , stem cell , immunology , genetics
Background and Objectives Previously, a weak phenotype A m or B m was assumed to be caused by a reduction of A or B gene expression in bone marrow cells, but not in mucus‐secreting cells. However, ABO expression has not been examined in erythroid progenitor cells of A m or B m individuals. Materials and Methods We carried out in vitro erythroid differentiation of CD 34 + cells from peripheral blood of a B m individual harbouring a 3·0‐kb deletion including an erythroid cell‐specific regulatory element, named the +5·8‐kb site, in intron 1 of the human ABO blood group gene. Results During the in vitro differentiation of CD 34 + cells from this B m individual into erythroid cells, B‐antigens were not detectable on the cultured cells by flow cytometric analysis, and allele‐specific RT ‐ PCR consistently detected the transcripts from the O allele, but not from the B allele. Moreover, chromatin immunoprecipitation assay demonstrated that both RUNX 1 and GATA ‐2 or GATA ‐1 were bound to the +5·8‐kb site in cultured erythroid cells expressing ABO . Conclusion It is likely that the +5·8‐kb site enhances transcription from the ABO promoter in erythroid cells through binding of RUNX 1 and GATA ‐2 or GATA ‐1.