Analysis of Ets1 bound regions using ChIP-seq
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE83758 | GEO | 2016/12/31
SECONDARY ACCESSION(S): PRJNA327035
REPOSITORIES: GEO
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Project description:Natural killer (NK) cells are innate lymphoid cells that play a critical role in the direct immune defense against tumor cells and pathogens, and additionally have important immune regulatory functions by cytokine secretion. Whereas NK cell biology has been extensively studied in mouse models, transcriptional control of human NK cell differentiation is poorly understood. In this study, we generated ETS1-deficient human embryonic stem cell (hESC) clones using the CRISPR/Cas9 technology. In a complementary approach, we generated ETS1 loss-of-function cord blood hematopoietic stem cells (HSCs) by retroviral transduction of the dominant-negative ETS1 p27 isoform. We show that the transcription factor ETS1 is required for human NK cell differentiation. Transcriptome and ChIP analysis reveal that ETS1 directly regulates expression of several NK cell-linked transcription factors. Also, expression of genes involved in cytokine secretion and cytotoxic activity is ETS1-dependent, whereby these effector functions are decreased in residual NK cells developing from ETS1 loss-of-function cord blood hematopoietic stem cells. Our data show that ETS1 is a critical regulator of human NK cell development and function, and provide important insights in the underlying molecular mechanisms.
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Project description:Natural killer (NK) cells are innate lymphoid cells that play a critical role in the direct immune defense against tumor cells and pathogens, and additionally have important immune regulatory functions by cytokine secretion. Whereas NK cell biology has been extensively studied in mouse models, transcriptional control of human NK cell differentiation is poorly understood. In this study, we generated ETS1-deficient human embryonic stem cell (hESC) clones using the CRISPR/Cas9 technology. In a complementary approach, we generated ETS1 loss-of-function cord blood hematopoietic stem cells (HSCs) by retroviral transduction of the dominant-negative ETS1 p27 isoform. We show that the transcription factor ETS1 is required for human NK cell differentiation. Transcriptome and ChIP analysis reveal that ETS1 directly regulates expression of several NK cell-linked transcription factors. Also, expression of genes involved in cytokine secretion and cytotoxic activity is ETS1-dependent, whereby these effector functions are decreased in residual NK cells developing from ETS1 loss-of-function cord blood hematopoietic stem cells. Our data show that ETS1 is a critical regulator of human NK cell development and function, and provide important insights in the underlying molecular mechanisms.
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Project description:Angiogenesis is a highly orchestrated process involving complex crosstalk between several endothelial cell (EC) processes including cell cycle, cell survival and migration. Transcription factors ETS1 and ETS2 are required for EC functions necessary for embryonic angiogenesis. However owing to the lethal nature of the double mutant embryo, the specific gene targets of these factors are yet to be identified. In the current study, we try to elucidate the effect of endothelial cell specific deletion of Ets1 and Ets2 on post natal angiogenesis and characterize the downstream regulatory pathways. Deletion of Ets1 and Ets2, restricted to endothelial cells in new born mice (P1-P3), reduced retinal angiogenesis. Similarly, EC infiltration and invasion into matrigel plugs subsided when matrigel admixed with mouse mammary tumor cells was injected into adult mice with inactivated Ets1 and Ets2 specifically in ECs. Expression of key cell cycle and cell survival regulators were diminished in double mutant cells as compared to controls. In addition, both these factors were found to occupy the enhancer regions of the target genes. Deletion of Ets1 and Ets2 in cultured aortic EC resulted in altered cell cycle phases with a G2/M phase arrest and increased sensitivity to apoptosis in vitro. These results demonstrate that deletion of Ets1 and Ets2 in endothelial cells inhibits angiogenesis by altering cell cycle progression and decreasing cell survival.
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Project description:We performed microarray analysis of gene expression in WT and Ets1-/- CD4+ CD8+ DP thymocytes. Overall, we find that Ets1-/- thymocytes display gene expression signatures closer to previous stages of thymocyte development (e.g. DN3-4) than WT DP cells, suggesting that while these cells do become DP thymocytes in the absence of Ets1, that the latter is required for the upregulation of later T-cell genes and that its presence is required for the downregulation of genes corresponding to earlier and alternative stages of development.
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