TFII-I/Gtf2i and Erythro-Megakaryopoiesis

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

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)

Abstract

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.

Original languageEnglish
Article number590180
JournalFrontiers in Physiology
Volume11
DOIs
Publication statusPublished - 25 Sept 2020

Keywords

  • erythropoiesis
  • globin
  • Gtf2i
  • megakaryopoiesis
  • TFII-I
  • transcription factor

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