GATA-1 and c-myb crosstalk during red blood cell differentiation through GATA-1 binding sites in the c-myb promoter

Bartůněk, Petr; Králová, Jarmila; Blendinger, Gitta; Dvořák, Michal; Zenke, Martin

doi:10.1038/sj.onc.1206281

Cited by 60 publications

(41 citation statements)

References 58 publications

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“…In contrast, constitutive expression of c-Myb has been reported to block erythrocyte maturation (53,54). A more recent study using a dose-and timing-controlled gene expression system showed overexpression of c-Myb; however, it prevented the terminal differentiation of erythrocytes and megakaryocytes (37), indicating that appropriate levels of c-Myb protein are strictly defined at distinct development and differentiation steps of each hematopoietic cell lineage.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA miR-150 Is Involved in Vα14 Invariant NKT Cell Development and Function

Zheng

Zhou

2012

The Journal of Immunology

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CD1d-restricted Vα14 invariant NKT (iNKT) cells play an important role in the regulation of diverse immune responses. MicroRNA-mediated RNA interference is emerging as a crucial regulatory mechanism in the control of iNKT cell differentiation and function. Yet, roles of specific microRNAs in the development and function of iNKT cells remain to be further addressed. In this study, we identified the gradually increased expression of microRNA-150 (miR-150) during the maturation of iNKT cells in thymus. Using miR-150 knockout (KO) mice, we found that miR-150 deletion resulted in an interruption of iNKT cell final maturation in both thymus and periphery. Upon activation, iNKT cells from miR-150KO mice showed significantly increased IFN-γ production compared with wild-type iNKT cells. Bone marrow-transferring experiments demonstrated the cell-intrinsic characteristics of iNKT cell maturation and functional defects in mice lacking miR-150. Furthermore, miR-150 target c-Myb was significantly upregulated in miR-150KO iNKT cells, which potentially contribute to iNKT cell defects in miR-150KO mice. Our data define a specific role of miR-150 in the development and function of iNKT cells.

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Section: Discussionmentioning

confidence: 99%

MicroRNA miR-150 Is Involved in Vα14 Invariant NKT Cell Development and Function

Zheng

Zhou

2012

The Journal of Immunology

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“…GATA-1 directly represses numerous genes including Kit, Gata2, Myc, Myb, and others. [14][15][16]24,25,[52][53][54] In multipotential progenitors, the Kit and Gata2 loci are relatively highly expressed and are occupied by GATA-2. During erythroid maturation, GATA-1 replaces GATA-2 at these loci, coincident with down-regulated expression of these genes.…”

Section: Discussionmentioning

confidence: 99%

“…[14][15][16]24,25,[52][53][54] This property is important for normal hematopoiesis and may contribute to leukemia, as a subset of GATA-1 target genes is inadequately repressed in Down syndrome-associated acute megakaryoblastic leukemia, which expresses the amino-truncated mutant protein GATA-1s. 14,55,56 To study the GATA-1-regulated program of gene repression in MEPs, we used the binomial test for significance to examine overlap between the 300 genes most strongly downregulated by GATA-1 in G1ME cells and Gene Ontology functional classifications (http://www.geneontology.org).…”

Section: Gata-1 Represses a Myeloid Program By Inhibiting Pu1 Expresmentioning

confidence: 99%

Graded repression of PU.1/Sfpi1 gene transcription by GATA factors regulates hematopoietic cell fate

Chou

Khandros

Bailey

et al. 2009

Blood

102

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GATA-1 and PU.1 are essential hematopoietic transcription factors that control erythromegakaryocytic and myelolymphoid differentiation, respectively. These proteins antagonize each other through direct physical interaction to repress alternate lineage programs. We used immortalized Gata1 ؊ erythromegakaryocytic progenitor cells to study how PU.1/Sfpi1 expression is regulated by GATA-1 and GATA-2, a related factor that is normally expressed at earlier stages of hematopoi-

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“…c-Myb is expressed in early erythroid differentiated cells and is downregulated with differentiation by Gata1 in association with the transcription co-repressor FOG1. 48 It was proposed that c-Myb may also function as a Gata2 repressor because Gata2 expression levels were increased by fivefold in c-Myb KD/KD E14.5 FL cells, inducing an immature erythroid phenotype. 40 Furthermore, ERG is a direct repressor of c-myb as previously shown by ChiP-Seq and gene expression studies.…”

Section: Discussionmentioning

confidence: 99%

Perturbation of fetal hematopoiesis in a mouse model of Down syndrome’s transient myeloproliferative disorder

Birger

Goldberg

Chlon

et al. 2013

Blood

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Key Points• Transient expansion of fetal megaerythroid progenitors in ERG/Gata1s mouse is biologically similar to Down syndrome TMD.• The N-terminal domain of GATA1 and the downregulation of ERG expression are essential for normal fetal erythropoiesis.Children with Down syndrome develop a unique congenital clonal megakaryocytic proliferation disorder (transient myeloproliferative disorder [TMD]). It is caused by an expansion of fetal megakaryocyte-erythroid progenitors (MEPs) triggered by trisomy of chromosome 21 and is further enhanced by the somatic acquisition of a mutation in GATA1. These mutations result in the expression of a short-isoform GATA1s lacking the N-terminal domain. To examine the hypothesis that the Hsa21 ETS transcription factor ERG cooperates with GATA1s in this process, we generated double-transgenic mice expressing hERG and Gata1s. We show that increased expression of ERG by itself is sufficient to induce expansion of MEPs in fetal livers. Gata1s expression synergizes with ERG in enhancing the expansion of fetal MEPs and megakaryocytic precursors, resulting in hepatic fibrosis, transient postnatal thrombocytosis, anemia, a gene expression profile that is similar to that of human TMD and progression to progenitor myeloid leukemia by 3 months of age. This ERG/Gata1s transgenic mouse model also uncovers an essential role for the N terminus of Gata1 in erythropoiesis and the antagonistic role of ERG in fetal erythroid differentiation and survival. The human relevance of this finding is underscored by the recent discovery of similar mutations in GATA1 in patients with Diamond-Blackfan anemia. (Blood. 2013;122(6):988-998)

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GATA-1 and c-myb crosstalk during red blood cell differentiation through GATA-1 binding sites in the c-myb promoter

Cited by 60 publications

References 58 publications

MicroRNA miR-150 Is Involved in Vα14 Invariant NKT Cell Development and Function

MicroRNA miR-150 Is Involved in Vα14 Invariant NKT Cell Development and Function

Graded repression of PU.1/Sfpi1 gene transcription by GATA factors regulates hematopoietic cell fate

Perturbation of fetal hematopoiesis in a mouse model of Down syndrome’s transient myeloproliferative disorder

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