GATA-1 mediates auto-regulation of Gfi-1B transcription in K562 cells

Huang, Duen Yi

doi:10.1093/nar/gki838

Cited by 47 publications

(72 citation statements)

References 40 publications

(59 reference statements)

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“…In many hematopoietic subsets, the expression of the Gfi1 and Gfi1b genes can be autoregulated by the Gfi1 and Gfi1b proteins themselves. [13][14][15] Gfi1 may control the expression of the Gfi1b gene and vice versa, [16][17][18] although the biological relevance of this crossregulation is poorly understood as both proteins are expressed in certain cell types. Gfi1 and Gfi1b gene expression is co-regulated by other transcription factors such as Ajuba 19 and Ikaros 20 for Gfi1 and GATA1, NF-Y, Oct1 and HMGB2 for Gfi1b.…”

Section: Structure and Expression Regulation Of Gfi1 And Gfi1b Proteinsmentioning

confidence: 99%

“…Gfi1 and Gfi1b gene expression is co-regulated by other transcription factors such as Ajuba 19 and Ikaros 20 for Gfi1 and GATA1, NF-Y, Oct1 and HMGB2 for Gfi1b. 15,17,21 Gfi1 protein expression is also regulated by microRNAs. 22 Finally, Gfi1 expression is also regulated at the protein level through ubiquitin-proteasome-mediated degradation.…”

Section: Structure and Expression Regulation Of Gfi1 And Gfi1b Proteinsmentioning

confidence: 99%

“…15,18,29,32 Gfi1 and Gfi1b also interact physically with other transcription factors through their zinc fingers to co-regulate gene expression (Figures 1 and 2). 17,29,[33][34][35][36] For example, Gfi1 interacts directly with ETS1 to repress the Bax gene through adjacent DNA binding sites. 33 Gfi1 may also mediate repression independently of DNA binding through interactions with the transcription factors Miz-1 and Pu.1.…”

Section: Structure and Expression Regulation Of Gfi1 And Gfi1b Proteinsmentioning

confidence: 99%

“…34,35 Similarly, Gfi1b controls the activity of the transcription factor GATA1 through direct protein-protein interactions on the DNA. 17,37 Apart from transcription regulation, Gfi1 also regulates protein expression at another level. Gfi1 mediates alternative splicing of CD45 transcripts and thereby controls T-cell receptor signaling.…”

Section: Structure and Expression Regulation Of Gfi1 And Gfi1b Proteinsmentioning

confidence: 99%

“…Gfi1b is also part of a complex that contains several other transcription factors. 17,31,36 Gfi1 in neutropenia, myeloid leukemia and hyperinflammatory responses…”

Section: Biological Roles Of Gfi1 and Gfi1bmentioning

confidence: 99%

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Gfi1 and Gfi1b: key regulators of hematopoiesis

2010

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Transcription factor Growth factor independence 1 (Gfi1) is required for multilineage blood cell development, from stem and progenitor cells to differentiated lymphoid and myeloid cells. Gfi1 expression is rapidly induced by cytokines that control both the adaptive and innate immune systems. Gfi1 itself represses the expression of genes implicated in cell survival, proliferation and differentiation. Changes in Gfi1 expression and function have not only been implicated in neutropenia, allergy, autoimmunity and hyperinflammatory responses, but also in lymphoma and more recently in the development of leukemia. In this study, we review how Gfi1 and its paralogue Gfi1b control the development of blood cells, discuss how changes in Gfi1 and Gfi1b function contribute to hematological disease and report on the molecular function of these proteins.

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Section: Structure and Expression Regulation Of Gfi1 And Gfi1b Proteinsmentioning

confidence: 99%

Section: Structure and Expression Regulation Of Gfi1 And Gfi1b Proteinsmentioning

confidence: 99%

Section: Structure and Expression Regulation Of Gfi1 And Gfi1b Proteinsmentioning

confidence: 99%

Section: Structure and Expression Regulation Of Gfi1 And Gfi1b Proteinsmentioning

confidence: 99%

“…Gfi1b is also part of a complex that contains several other transcription factors. 17,31,36 Gfi1 in neutropenia, myeloid leukemia and hyperinflammatory responses…”

Section: Biological Roles Of Gfi1 and Gfi1bmentioning

confidence: 99%

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Gfi1 and Gfi1b: key regulators of hematopoiesis

2010

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Erythropoiesis: Model systems, molecular regulators, and developmental programs

2009

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SummaryHuman erythropoiesis is a complex multistep developmental process that begins at the level of pluripotent hematopoietic stem cells (HSCs) at bone marrow microenvironment (HSCs niche) and terminates with the production of erythrocytes (RBCs). This review covers the basic and contemporary aspects of erythropoiesis. These include the: (a) cell-lineage restricted pathways of differentiation originated from HSCs and going downward toward the blood cell development; (b) model systems employed to study erythropoiesis in culture (erythroleukemia cell lines and embryonic stem cells) and in vivo (knockout animals: avian, mice, zebrafish, and xenopus); (c) key regulators of erythropoiesis (iron, hypoxia, stress, and growth factors); (d) signaling pathways operating at hematopoietic stem cell niche for homeostatic regulation of self renewal (SCF/c-kit receptor, Wnt, Notch, and Hox) and for erythroid differentiation (HIF and EpoR). Furthermore, this review presents the mechanisms through which transcriptional factors (GATA-1, FOG-1, TAL-1/ SCL/MO2/Ldb1/E2A, EKLF, Gfi-1b, and BCL11A) and miRNAs regulate gene pattern expression during erythroid differentiation. New insights regarding the transcriptional regulation of a-and b-globin gene clusters were also presented. Emphasis was also given on (i) the developmental program of erythropoiesis, which consists of commitment to terminal erythroid maturation and hemoglobin production, (two closely coordinated events of erythropoieis) and (ii) the capacity of human embryonic and umbilical cord blood (UCB) stem cells to differentiate and produce RBCs in culture with highly selective media. These most recent developments will eventually permit customized red blood cell production needed for transfusion.

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Gfi-1B Promoter Remains Associated with Active Chromatin Marks Throughout Erythroid Differentiation of Human Primary Progenitor Cells

et al. 2009

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Growth Factor Independent-1B (Gfi-1B) is a transcriptional repressor that plays critical roles in the control of erythropoiesis and megakaryopoiesis. Gfi-1B expression was described to be repressed by an autoregulatory feedback control loop. Here, we show that Gfi-1 transcription is positively regulated early after induction of erythroid differentiation and remains highly active to late erythroblasts. Using chromatin immunoprecipitation assays in CD34+ cells from human cord blood, we found that Gfi-1 and GATA-2 in immature progenitors and then Gfi-1B and GATA-1 in erythroblasts are bound to the Gfi-1B promoter as well as to the promoter of c-myc, a known Gfi-1B target gene. Surprisingly, this Gfi-1/GATA-2–Gfi-1B/GATA-1 switch observed at erythroblast stages is associated to an increase in the Gfi-1B transcription whereas it triggers repression of c-myc transcription. Accordingly, analysis of chromatin modification patterns shows that HDAC, CoREST, and LSD1 are recruited to the c-myc promoter leading to appearance of repressive chromatin marks. In contrast, the Gfi-1B promoter remains associated with a transcriptionally active chromatin configuration as highlighted by an increase in histone H3 acetylation and concomitant release of the LSD1 and CoREST corepressors. The repressive function of Gfi-1B therefore depends on the nature of the proteins recruited to the target gene promoters and on chromatin modifications. We conclude that Gfi-1B behaves as a lineage-affiliated gene with an open chromatin configuration in multipotent progenitors and sustained activation as cells progress throughout erythroid differentiation.

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GATA-1 mediates auto-regulation of Gfi-1B transcription in K562 cells

Cited by 47 publications

References 40 publications

Gfi1 and Gfi1b: key regulators of hematopoiesis

Gfi1 and Gfi1b: key regulators of hematopoiesis

Erythropoiesis: Model systems, molecular regulators, and developmental programs

Gfi-1B Promoter Remains Associated with Active Chromatin Marks Throughout Erythroid Differentiation of Human Primary Progenitor Cells

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