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TFII-I/Gtf2i and Erythro-Megakaryopoiesis

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Aishwarya Gurumurthy, Qiong Wu, Rukiye Nar, Kimberly Paulsen, Alexis Trumbull, Ryan C. Fishman, Marjorie Brand, John Strouboulis, Zhijian Qian, Jörg Bungert

Original languageEnglish
Article number590180
JournalFrontiers in Physiology
Published25 Sep 2020

King's Authors


TFII-I is a ubiquitously expressed transcription factor that positively or negatively regulates gene expression. TFII-I has been implicated in neuronal and immunologic diseases as well as in thymic epithelial cancer. Williams–Beuren Syndrome (WBS) is caused by a large hemizygous deletion on chromosome 7q11.23 which encompasses 26–28 genes, including GTF2I, the human gene encoding TFII-I. A subset of WBS patients has recently been shown to present with macrocytosis, a mild anemia characterized by enlarged erythrocytes. We conditionally deleted the TFII-I/Gtf2i gene in adult mice by tamoxifen induced Cre-recombination. Bone marrow cells revealed defects in erythro-megakaryopoiesis and an increase in expression of the adult β-globin gene. The data show that TFII-I acts as a repressor of β–globin gene transcription and that it is implicated in the differentiation of erythro-megakaryocytic cells.

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