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Med23 serves as a gatekeeper of the myeloid potential of hematopoietic stem cells

ABSTRACT: Med23 serves as a gatekeeper of the myeloid potential of hematopoietic stem cells

PROVIDER: PRJNA438937 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6856310_1.fastq.gz	Fastqsanger.gz
	SRR6856310_2.fastq.gz	Fastqsanger.gz
	SRR6856311_1.fastq.gz	Fastqsanger.gz
	SRR6856311_2.fastq.gz	Fastqsanger.gz
	SRR6856312_1.fastq.gz	Fastqsanger.gz

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Med23 serves as a gatekeeper of the myeloid potential of hematopoietic stem cells

Project description:In response to myeloablative stresses, HSCs are rapidly activated to replenish myeloid progenitors, while maintaining full potential of self-renewal to ensure life-long hematopoiesis. However, the key factors that orchestrate HSC activities during physiological stresses remain largely unknown. Here we report that Med23 controls the myeloid potential of activated HSCs. Ablation of Med23 in hematopoietic system leads to lymphocytopenia. Med23- deficient HSCs undergo myeloid-biased differentiation and lose the self-renewal capacity. Interestingly, Med23-deficient HSCs are much easier to be activated in response to physio- logical stresses. Mechanistically, Med23 plays essential roles in maintaining stemness genes expression and suppressing myeloid lineage genes expression. Med23 is downregulated in HSCs and Med23 deletion results in better survival under myeloablative stress. Altogether, our findings identify Med23 as a gatekeeper of myeloid potential of HSCs, thus providing unique insights into the relationship among Med23-mediated transcriptional regulations, the myeloid potential of HSCs and HSC activation upon stresses.

2018-07-14 | GSE112008 | GEO

The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells (RNA-Seq)

Project description:To ensure the rapid response to stimuli, some HSCs are specifically prepared (primed) for tasks involving activation and reconstitution. However, the key factors that regulate the primed state of HSCs are largely unknown. Here we report that Med23 controls the formation of myeloid-primed HSCs. Ablation of Med23 in hematopoietic system leads to lymphocytopenia. Moreover, Med23-deficient HSCs undergo myeloid-biased differentiation and lose the self-renewal capacity. Interestingly, Med23-deficient HSCs are in myeloid-primed state and are much easier to be activated in response to physiological stresses. Mechanistically, Med23 plays essential roles in maintaining stemness genes expression and suppressing myeloid lineage genes expression. Med23 is down-regulated in HSCs and Med23 deletion results in better survival under myeloablative stress. Altogether, our findings identified Med23 as a gatekeeper of the myeloid-primed state of HSCs, thus providing unique insights into the relationship among Med23-mediated transcriptional regulations, the myeloid-primed state of HSCs and HSC activation upon stresses.

2018-07-15 | GSE112358 | GEO

The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells (ATAC-Seq)

2018-07-15 | GSE112357 | GEO

The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells

Project description:The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells

| PRJNA445738 | ENA

Med23 serves as a gatekeeper of the myeloid potential of hematopoietic stem cells.

Project description:In response to myeloablative stresses, HSCs are rapidly activated to replenish myeloid progenitors, while maintaining full potential of self-renewal to ensure life-long hematopoiesis. However, the key factors that orchestrate HSC activities during physiological stresses remain largely unknown. Here we report that Med23 controls the myeloid potential of activated HSCs. Ablation of Med23 in hematopoietic system leads to lymphocytopenia. Med23-deficient HSCs undergo myeloid-biased differentiation and lose the self-renewal capacity. Interestingly, Med23-deficient HSCs are much easier to be activated in response to physiological stresses. Mechanistically, Med23 plays essential roles in maintaining stemness genes expression and suppressing myeloid lineage genes expression. Med23 is downregulated in HSCs and Med23 deletion results in better survival under myeloablative stress. Altogether, our findings identify Med23 as a gatekeeper of myeloid potential of HSCs, thus providing unique insights into the relationship among Med23-mediated transcriptional regulations, the myeloid potential of HSCs and HSC activation upon stresses.

| S-EPMC6138688 | biostudies-literature

The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells (ATAC-Seq)

Project description:The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells (ATAC-Seq)

| PRJNA445739 | ENA

The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells (RNA-Seq)

Project description:The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells (RNA-Seq)

| PRJNA445740 | ENA

The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-07-15 | GSE112359 | GEO

MEF wt versus Med23-/- KO after 20% Serum Stimulation

Project description:Affymetrix MOE430A arrays. Mouse embryonic fibroblasts (MEFs) from E11 passaged through crisis. Starved in 0.5% FBS for 16 h then stimulated by 20% serum final concentration for 30 minutes. The purpose was to identify genes affected by the loss of MED23 protein (subunit of the mediator complex). Samples were assayed in duplicate (Set 1 and Set 2) for starved state and serum state cells. Cells starved in low-serum (0.5%) for 16 h then add final conc. 20% FBS for 30 minutes. Harvest total RNA from duplicate samples. One sample set is kept starved and serves as the baseline. The other set is stimulated. This is done for both wild-type cell and the Med23-/- KO cells. We looked for gene expression fold changes greater than 2 (plus or minus) to find genes affected for serum stimulation by the loss of MED23, looking in detail at immediate early genes like Egr1.

2009-04-14 | E-GEOD-15638 | biostudies-arrayexpress

Med23-dependent gene expression programs in T cells

Project description:To analysis TCR induced Med23-dependent gene expression programs in T cells, we have employed microarray expression profiling as a discovery platform to identify genes with the potential to be regulated by Med23 in unstimulated or stimulated T cells. Mice CD4 T cells from wildtype and Med23 knockout mice were left unstimulated or stimulated for 6 hr, and gene expression difference was identified among four samples. Expression of seven genes (Med23, IFNg, IL2, Egr2, c-Fos, c-Jun and Foxp1) was validated in the same RNA samples by real-time PCR. TCR induced Med23-dependent gene expression was measured after unstimulation or stimulation for 6 hr in wildtype and Med23 knockout CD4 T cells.

2014-08-27 | E-GEOD-60779 | biostudies-arrayexpress

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