Establishment of erythroleukemic <scp>GAK</scp>14 cells and characterization of <scp>GATA</scp>1 <scp>N</scp>‐terminal domain

Mukai, Harumi Y.; Suzuki, Mikiko; Nagano, Masumi; Ohmori, Shingo; Otsuki, Akihito; Tsuchida, Kouhei; Moriguchi, Takashi; Ohneda, Kinuko; Shimizu, Ritsuko; Onodera, Osamu; Yamamoto, Masayuki

doi:10.1111/gtc.12084

Cited by 4 publications

(6 citation statements)

References 41 publications

(89 reference statements)

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“…Although the transduced GATA1 expression level in GKG cells is comparable to that in mouse erythroleukemia (MEL) cells, these cells sustain their immature morphology on OP9 stromal cells (Fig. A, right panel) and start to differentiate into mature erythroid cells upon the co‐culture with the fetal liver‐derived stromal cells (Mukai et al ., ). GAK14 cells express GATA2 abundantly, but the GATA1 expression was hardly detected (Fig.…”

Section: Resultsmentioning

confidence: 97%

“…Therefore, we surmised that GATA factor switching contributes to the selection of binding sites by GATA1. To examine whether GATA1-binding sites widely overlapped with GATA2-binding sites or not, we carried out GATA2 and GATA1 ChIP-chip analyses using a Gata1 knockdown proerythroblast-like cell line (GAK14) and the corresponding cell line, named GKG cells, supplemented with exogenous GATA1 into the parental GAK14 cells (Mukai et al, 2013). GAK14 cells are established from spleens of the Gata1 G1.05/X mouse developing erythroblastic leukemia, whose morphology resembles that of the (Shimizu et al 2004).…”

Section: Gfp-bright Cells From Gata1 G105/y Embryos Fail To Differenmentioning

confidence: 99%

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GATA factor switching from GATA2 to GATA1 contributes to erythroid differentiation

et al. 2013

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Transcription factor GATA2 is highly expressed in hematopoietic stem cells and progenitors, whereas its expression declines after erythroid commitment of progenitors. In contrast, the start of GATA1 expression coincides with the erythroid commitment and increases along with the erythroid differentiation. We refer this dynamic transition of GATA factor expression to as the 'GATA factor switching'. Here, we examined contribution of the GATA factor switching to the erythroid differentiation. In Gata1-knockdown embryos that concomitantly express Gata2-GFP reporter, high-level expression of GFP reporter was detected in accumulated immature hematopoietic cells with impaired differentiation, demonstrating that GATA1 represses Gata2 gene expression in hematopoietic progenitors in vivo. We have conducted chromatin immunoprecipitation (ChIP) on microarray analyses of GATA2 and GATA1, and results indicate that the GATA1-binding sites widely overlap with the sites pre-occupied by GATA2 before the GATA1 expression. Importantly, erythroid genes harboring GATA boxes bound by both GATA1 and GATA2 tend to be expressed in immature erythroid cells, whereas those harboring GATA boxes to which GATA1 binds highly but GATA2 binds only weakly are important for the mature erythroid cell function. Our results thus support the contention that preceding binding of GATA2 helps the following binding of GATA1 and thereby secures smooth expression of the transient-phase genes.

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Section: Resultsmentioning

confidence: 97%

Section: Gfp-bright Cells From Gata1 G105/y Embryos Fail To Differenmentioning

confidence: 99%

GATA factor switching from GATA2 to GATA1 contributes to erythroid differentiation

et al. 2013

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“…Genes erythroleukemia cells were able to differentiate into mature erythrocytes when complemented with full-length Gata1 (ref. 45 ). In contrast to Gata1 1.05/+ mice, Nsd1 −/− mice developed a fully penetrant erythroleukemia-like phenotype after a shorter latency (Fig.…”

Section: Inputmentioning

confidence: 99%

Nuclear interacting SET domain protein 1 inactivation impairs GATA1-regulated erythroid differentiation and causes erythroleukemia

et al. 2020

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The nuclear receptor binding SET domain protein 1 (NSD1) is recurrently mutated in human cancers including acute leukemia. We show that NSD1 knockdown alters erythroid clonogenic growth of human CD34 + hematopoietic cells. Ablation of Nsd1 in the hematopoietic system of mice induces a transplantable erythroleukemia. In vitro differentiation of Nsd1 −/− erythroblasts is majorly impaired despite abundant expression of GATA1, the transcriptional master regulator of erythropoiesis, and associated with an impaired activation of GATA1induced targets. Retroviral expression of wildtype NSD1, but not a catalytically-inactive NSD1 N1918Q SET-domain mutant induces terminal maturation of Nsd1 −/− erythroblasts. Despite similar GATA1 protein levels, exogenous NSD1 but not NSD N1918Q significantly increases the occupancy of GATA1 at target genes and their expression. Notably, exogenous NSD1 reduces the association of GATA1 with the co-repressor SKI, and knockdown of SKI induces differentiation of Nsd1 −/− erythroblasts. Collectively, we identify the NSD1 methyltransferase as a regulator of GATA1-controlled erythroid differentiation and leukemogenesis.

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“…GATA-switching site at -77, -3.9, -2.8, and -1.8 kb and the 4th intronic ?9.5 kb (Gata2 VE; vascular enhancer) regions are indicated established from erythroleukemia cells spontaneously developed in Gata1 gene knockdown heterozygous female (Gata1 G1.05/? ) mice [47]. GAK14 cells actively proliferate as immature erythroid progenitors.…”

Section: Gata Switching Underlies Erythropoiesismentioning

confidence: 99%

A regulatory network governing Gata1 and Gata2 gene transcription orchestrates erythroid lineage differentiation

Moriguchi

Yamamoto

2014

Int J Hematol

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GATA transcription factor family members GATA1 and GATA2 play crucial roles in the regulation of lineage-restricted genes during erythroid differentiation. GATA1 is indispensable for survival and terminal differentiation of erythroid, megakaryocytic and eosinophilic progenitors, whereas GATA2 regulates proliferation and maintenance of hematopoietic stem and progenitor cells. Expression levels of GATA1 and GATA2 are primarily regulated at the transcriptional level through auto-and reciprocal regulatory networks formed by these GATA factors. The dynamic and strictly controlled change of expression from GATA2 to GATA1 during erythropoiesis has been referred to as GATA factor switching, which plays a crucial role in erythropoiesis. The regulatory network comprising GATA1 and GATA2 gives rise to the stage-specific changes in Gata1 and Gata2 gene expression during erythroid differentiation, which ensures specific expression of early and late erythroid genes at each stage. Recent studies have also shed light on the genome-wide binding profiles of GATA1 and GATA2, and the significance of epigenetic modification of Gata1 gene during erythroid differentiation. This review summarizes the current understanding of network regulation underlying stagedependent Gata1 and Gata2 gene expressions and the functional contribution of these GATA factors in erythroid differentiation.

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Establishment of erythroleukemic GAK14 cells and characterization of GATA1 N‐terminal domain

Cited by 4 publications

References 41 publications

GATA factor switching from GATA2 to GATA1 contributes to erythroid differentiation

GATA factor switching from GATA2 to GATA1 contributes to erythroid differentiation

Nuclear interacting SET domain protein 1 inactivation impairs GATA1-regulated erythroid differentiation and causes erythroleukemia

A regulatory network governing Gata1 and Gata2 gene transcription orchestrates erythroid lineage differentiation

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