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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE112359 | GEO | 2018/07/15

REPOSITORIES: GEO

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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

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

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

| PRJNA445738 | ENA

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

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

Crystal structure of human Mediator subunit MED23.

Project description:The Mediator complex transduces regulatory information from enhancers to promoters and performs essential roles in the initiation of transcription in eukaryotes. Human Mediator comprises 26 subunits forming three modules termed Head, Middle and Tail. Here we present the 2.8 Å crystal structure of MED23, the largest subunit from the human Tail module. The structure identifies 25 HEAT repeats-like motifs organized into 5 α-solenoids. MED23 adopts an arch-shaped conformation, with an N-terminal domain (Nter) protruding from a large core region. In the core four solenoids, motifs wrap on themselves, creating triangular-shaped structural motifs on both faces of the arch, with extended grooves propagating through the interfaces between the solenoid motifs. MED23 is known to interact with several specific transcription activators and is involved in splicing, elongation, and post-transcriptional events. The structure rationalizes previous biochemical observations and paves the way for improved understanding of the cross-talk between Mediator and transcriptional activators.

| S-EPMC6107663 | biostudies-literature

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

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

| PRJNA438937 | ENA

Mediator complex regulates alternative mRNA processing via the MED23 subunit.

Project description:Mediator complex is an integrative hub for transcriptional regulation. Here we show that Mediator regulates alternative mRNA processing via its MED23 subunit. Combining tandem affinity purification and mass spectrometry, we identified a number of mRNA processing factors that bind to a soluble recombinant Mediator subunit, MED23, but not to several other Mediator components. One of these factors, hnRNP L, specifically interacts with MED23 in vitro and in vivo. Consistently, Mediator partially colocalizes with hnRNP L and the splicing machinery in the cell. Functionally, MED23 regulates a subset of hnRNP L-targeted alternative splicing (AS) and alternative cleavage and polyadenylation (APA) events, as shown by minigene reporters and exon array analysis. ChIP-seq analysis revealed that MED23 can regulate hnRNP L occupancy at their coregulated genes. Taken together, these results demonstrate a crosstalk between Mediator and the splicing machinery, providing a molecular basis for coupling mRNA processing to transcription.

| S-EPMC3288850 | biostudies-literature

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