KLF1 stabilizes GATA-1 and TAL1 occupancy in the human β-globin locus

Kang, Young-Seok; Kim, Yea Woon; Yun, Jangmi; Shin, Jisoo; Kim, AeRi

doi:10.1016/j.bbagrm.2014.12.010

Cited by 29 publications

(19 citation statements)

References 39 publications

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“…GATA1 and the myeloid transcription factor PU.1 have been reported to physically interact in antagonizing each other's functions by displacing other protein cofactors and/or preventing DNA binding, thus influencing cell lineage commitment decisions and activation of associated transcription programs ( and references therein). GATA1 also interacts in erythroid cells with other transcription factors such as KLF1, SP1, and GFI1B, as well as with chromatin remodeling factors such as ACF/WCRF, BRG1 and pRB/E2F . Lastly, GATA1 interacts with the CBP/p300 histone acetyltransferase, which mediates acetylation of the GATA1 ZnFs, modulating its DNA binding properties and/or protein stability (see below) …”

Section: Gata1 Functions In Erythropoiesismentioning

confidence: 99%

Regulation of GATA1 levels in erythropoiesis

et al. 2019

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GATA1 is considered as the "master" transcription factor in erythropoiesis. It regulates at the transcriptional level all aspects of erythroid maturation and function, as revealed by gene knockout studies in mice and by genome-wide occupancies in erythroid cells. The GATA1 protein contains two zinc finger domains and an N-terminal transactivation domain. GATA1 translation results in the production of the full-length protein and of a shorter variant (GATA1s) lacking the N-terminal transactivation domain, which is functionally deficient in supporting erythropoiesis. GATA1 protein abundance is highly regulated in erythroid cells at different levels, including transcription, mRNA translation, posttranslational modifications, and protein degradation, in a differentiationstage-specific manner. Maintaining high GATA1 protein levels is essential in the early stages of erythroid maturation, whereas downregulating GATA1 protein levels is a necessary step in terminal erythroid differentiation. The importance of maintaining proper GATA1 protein homeostasis in erythropoiesis is demonstrated by the fact that both GATA1 loss and its overexpression result in lethal anemia. Importantly, alterations in any of those GATA1 regulatory checkpoints have been recognized as an important cause of hematological disorders such as dyserythropoiesis (with or without thrombocytopenia), β-thalassemia, Diamond-Blackfan anemia, myelodysplasia, or leukemia. In this review, we provide an overview of the multilevel regulation of GATA1 protein homeostasis in erythropoiesis and of its deregulation in hematological disease. K E Y W O R D S

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Section: Gata1 Functions In Erythropoiesismentioning

confidence: 99%

Regulation of GATA1 levels in erythropoiesis

et al. 2019

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“…The effect of cell differentiation is often associated with the dysfunction of the transcription factors in the signal transduction pathway. GATAbinding factor 1 (GATA-1), NF-E2, T-cell acute lymphocytic leukemia protein 1 (TAL1) and Kruppel like factor 1 (KLF1) are major erythroid-specific transcription activators that bind to the β-globin locus and regulate transcription of the globin gene (24). GATA-1 is a major regulator of the expression of other erythroid-specific activators in human erythroid K562 cells.…”

Section: Discussionmentioning

confidence: 99%

Induction of apoptosis and erythroid differentiation of human chronic myelogenous leukemia K562 cells by low concentrations of lidamycin

Zhang

Guo

et al. 2018

Oncol Rep

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Apoptosis induction and differentiation of promyelocytic leukemic cells into mature cells are major strategies for the drug-based treatment of leukemia. Lidamycin (LDM) which is a member of the enediyne antibiotic family exhibits extreme cytotoxicity. In the present study, the induction of apoptosis and differentiation in human chronic myeloid leukemia K562 cells by low concentrations of lidamycin were investigated. K562 cells were treated with lidamycin at various concentrations for 48 h, and accumulated in the metaphase as determined in previous experiments. Cell viability was determined using a Cell Counting Kit-8 (CCK-8) assay and the IC 50 value of lidamycin was 0.1±3.2 nM. Induction of apoptosis was investigated morphologically by acridine orange/ethidium bromide (AO/EtBr) staining. Growth inhibition and apoptosis induction were observed in cells treated with low concentrations of lidamycin. In addition, western blot analysis revealed that treatment of the K562 cells with lidamycin at low concentrations upregulated the expression of caspase-8 and caspase-3. The induction of differentiation in human chronic myeloid leukemia K562 cells by lidamycin at low concentrations was also investigated. The nitroblue tetrazolium reduction ability of K562 cells was increased following treatment with lidamycin. Low concentrations of lidamycin triggered erythroid differentiation among K562 cells, indicated by morphological changes, increased hemoglobin content, and the expression of cell surface antigens such as CD71. Additionally the expression of GATA-binding factor 1 (GATA-1) protein in low concentration lidamycin-treated K562 cells was increased. The results of the present study suggest that a low-concentration lidamycin exerts effects on apoptosis and erythroid differentiation induction by increasing the expression of caspases and GATA-1 protein. Lidamycin may serve a positive role in relevant targeted chemotherapy and may represent a potential candidate for chronic myelogenous leukemia differentiation-inducing treatment.

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“…To investigate the biological significance of these loops in ProEBs, we first conducted unbiased, de novo motif discovery analysis using DNA sequences from all HiChIP anchor regions. Strikingly, we identified an enrichment of consensus motifs of multiple TFs known to regulate specification of the erythroid lineage, including STAT (Kisseleva et al, 2002;Watowich, 2011), KLF (Cantor and Orkin, 2002;Kang et al, 2015;Miller and Bieker, 1993), and GATA (Cantor and Orkin, 2002;Lentjes et al, 2016;Weiss and Orkin, 1995) (Fig. 4A).…”

Section: Epo Regulates Transcription In a Pre-established Chromatin Cmentioning

confidence: 97%

Erythropoietin regulates transcription and YY1 dynamics in a pre-established chromatin architecture

Perreault

Brown

Venters

2020

Preprint

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The three dimensional architecture of the genome plays an essential role in establishing and maintaining cell identity. By contrast, the magnitude and temporal kinetics of changes in chromatin structure that arise during cell differentiation remain poorly understood. Here, we leverage a murine model of erythropoiesis to study the relationship between chromatin conformation, the epigenome, and transcription in erythroid cells. We discover that acute transcriptional responses induced by erythropoietin (EPO), the hormone necessary for erythroid differentiation, occur within an invariant chromatin topology. Within this pre-established landscape, Yin Yang 1 (YY1) occupancy dynamically redistributes to sites in proximity to EPOregulated genes. Using HiChIP, we identify chromatin contacts mediated by H3K27ac and YY1 that are enriched for enhancer-promoter interactions of EPO-responsive genes. Taken together, these data are consistent with an emerging model that rapid, signal-dependent transcription occurs in the context of a pre-established chromatin architecture.

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KLF1 stabilizes GATA-1 and TAL1 occupancy in the human β-globin locus

Cited by 29 publications

References 39 publications

Regulation of GATA1 levels in erythropoiesis

Regulation of GATA1 levels in erythropoiesis

Induction of apoptosis and erythroid differentiation of human chronic myelogenous leukemia K562 cells by low concentrations of lidamycin

Erythropoietin regulates transcription and YY1 dynamics in a pre-established chromatin architecture

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