Chromatin factor YY1 controls fetal hematopoietic stem cell migration and engraftment in mice [RNA-seq]
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ABSTRACT:
PROVIDER: PRJNA1174800 | ENA |
REPOSITORIES: ENA
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Project description:Fetal liver is a major organ for generating hematopoietic stem cells (HSCs) during embryonic development. Many questions remain unanswered regarding how transition of hematopoiesis from the fetal liver to the bone marrow (BM) is regulated. We demonstrate that mammalian Polycomb Group (PcG) protein Yin Yang 1 (YY1) is required for this transition, as conditional knockout of Yy1 in the hematopoietic system during fetal development results in exhaustion of fetal HSC pools and is associated with neonatal death. Yy1 deficient fetal HSCs have diminished capacity to migrate to and engraft the adult BM, and consequently fail to reconstitute blood. The genetic networks governing cell motility and adhesion are distinctly deregulated by YY1 knockout in fetal HSPCs. Notably, YY1 regulates mobility of fetal HSPCs largely through an indirect mechanism as it does not directly bind to the promoters of dysregulated genes involved in control of cell mobility. Instead, it regulates broader transcriptional mechanisms by regulating the genes in chromatin remodeling complexes and modulating chromatin accessibility that impact HSPC migration. Our study provides a framework to further decipher how temporal epigenomic configurations determine HSC fetal-to-adult transition during development.
2025-07-11 | GSE298778 | GEO
Project description:Fetal liver is a major organ for generating hematopoietic stem cells (HSCs) during embryonic development. Many questions remain unanswered regarding how transition of hematopoiesis from the fetal liver to the bone marrow (BM) is regulated. We demonstrate that mammalian Polycomb Group (PcG) protein Yin Yang 1 (YY1) is required for this transition, as a conditional knockout of Yy1 in the hematopoietic system during fetal development results in exhaustion of fetal HSC pools and neonatal death. Yy1 deficient fetal HSCs have diminished capacity to migrate to and engraft the adult BM, and consequently fail to reconstitute blood. YY1 deficiency leads to distinct transcriptomic changes in fetal hematopoietic stem progenitor cells (HSPCs) compared with adult HSPCs. The genetic networks governing cell motility and adhesion are distinctly deregulated by YY1 in fetal HSPCs. Notably, YY1 regulates mobility of fetal HSPCs largely through an indirect mechanism as it does not directly bind to the promoters of dysregulated genes involved in control of mobility. Instead, it regulates broader transcriptional mechanisms by modulating the genes in chromatin remodeling complexes that impact HSPC mobility. Our study provides a framework to further decipher how temporal epigenomic configurations determine HSC fetal-to-adult transition during development.
2025-07-11 | GSE279863 | GEO
Project description:Fetal liver is a major organ for generating hematopoietic stem cells (HSCs) during embryonic development. Many questions remain unanswered regarding how transition of hematopoiesis from the fetal liver to the bone marrow (BM) is regulated. We demonstrate that mammalian Polycomb Group (PcG) protein Yin Yang 1 (YY1) is required for this transition, as a conditional knockout of Yy1 in the hematopoietic system during fetal development results in exhaustion of fetal HSC pools and neonatal death. Yy1 deficient fetal HSCs have diminished capacity to migrate to and engraft the adult BM, and consequently fail to reconstitute blood. YY1 deficiency leads to distinct transcriptomic changes in fetal hematopoietic stem progenitor cells (HSPCs) compared with adult HSPCs. The genetic networks governing cell motility and adhesion are distinctly deregulated by YY1 in fetal HSPCs. Notably, YY1 regulates mobility of fetal HSPCs largely through an indirect mechanism as it does not directly bind to the promoters of dysregulated genes involved in control of mobility. Instead, it regulates broader transcriptional mechanisms by modulating the genes in chromatin remodeling complexes that impact HSPC mobility. Our study provides a framework to further decipher how temporal epigenomic configurations determine HSC fetal-to-adult transition during development.
2025-07-11 | GSE279864 | GEO
Project description:Chromatin factor YY1 controls fetal hematopoietic stem cell migration and engraftment in mice [ATAC-seq]
| PRJNA1271089 | ENA
Project description:Chromatin factor YY1 controls fetal hematopoietic stem cell migration and engraftment in mice [CUT&Tag]
| PRJNA1174796 | ENA
Project description:Human hematopoietic stem cell engraftment in goat
| PRJNA90277 | ENA
Project description:Quantitative proteomic analysis of mouse fetal and adult hematopoietic progenitor cells using TMT6plex and an SPS-MS3 method.
2020-07-02 | MSV000085672 | MassIVE
Project description:The protein Yin-Yang 1 (YY1) is a ubiquitous multifunctional transcription factor. Interestingly, there are several cellular functions controlled by YY1 that could play a role in Leishmania pathogenesis. Leishmaniasis is a human disease caused by protozoan parasites of the genus Leishmania. This study examined the potential role of macrophage YY1 in promoting Leishmania intracellular survival. Knockdown of YY1 resulted in attenuated survival of Leishmania in infected macrophages, suggesting a role of YY1 in Leishmania persistence. Biochemical fractionation studies revealed Leishmania infection caused redistribution of YY1 to the cytoplasm from the nucleus where it is primarily located. Inhibition of nuclear transport by leptomycin B attenuates infection-mediated YY1 redistribution and reduces Leishmania survival. This suggests that Leishmania induces the translocation of YY1 from the nucleus to the cytoplasm of infected cells, where it may regulate host molecules to favour parasite survival. A label-free quantitative whole proteome approach showed that the expression of a large number of macrophage proteins was dependent on the YY1 level. Interestingly, several of these proteins were modulated in Leishmania-infected cells, revealing YY1-dependent host response and suggesting their potential role in Leishmania pathogenesis. Together, these findings identify YY1 as a novel and essential virulence factor by proxy that promotes Leishmania survival.
2025-03-14 | PXD059968 | Pride
Project description:Advances in pluripotent stem cell and reprogramming technologies have given hope of generating hematopoietic stem cells (HSC) in culture. To succeed, greater understanding of the self-renewing HSC during human development is required. We discovered that glycophosphatidylinositol-anchored surface protein GPI-80 (Vanin 2) defines a distinct subpopulation of human fetal hematopoietic stem/progenitor cells (HSPC) with self-renewal ability. CD34+CD90+CD38-GPI-80+ HSPC were the sole population that maintained proliferative potential and undifferentiated state in bone marrow stroma co-culture, and engrafted in immunodeficient mice. GPI-80 expression also enabled tracking of HSC migration between human fetal hematopoietic niches. The most highly enriched surface protein in GPI-80+ HSPC as compared to their progeny was Integrin alpha-M (ITGAM), which in leukocytes cooperates with GPI-80 to support migration. Knockdown of either GPI-80 or ITGAM was sufficient to perturb undifferentiated HSPC in stroma co-culture. These findings indicate that human fetal HSC utilize common mechanisms with leukocytes for cell-cell interactions governing HSC self-renewal. We used microarrays to identify genes enriched in the GPI-80+ hematopoietic stem and progenitor population in fetal liver. RNA was extracted from enriched fetal liver hematopoietic stem and progenitor cells, and downstream progenitors, for comparison based on Affymetrix arrays.
2015-01-23 | E-GEOD-54315 | biostudies-arrayexpress
Project description:Advances in pluripotent stem cell and reprogramming technologies have given hope of generating hematopoietic stem cells (HSC) in culture. To succeed, greater understanding of the self-renewing HSC during human development is required. We discovered that glycophosphatidylinositol-anchored surface protein GPI-80 (Vanin 2) defines a distinct subpopulation of human fetal hematopoietic stem/progenitor cells (HSPC) with self-renewal ability. CD34+CD90+CD38-GPI-80+ HSPC were the sole population that maintained proliferative potential and undifferentiated state in bone marrow stroma co-culture, and engrafted in immunodeficient mice. GPI-80 expression also enabled tracking of HSC migration between human fetal hematopoietic niches. The most highly enriched surface protein in GPI-80+ HSPC as compared to their progeny was Integrin alpha-M (ITGAM), which in leukocytes cooperates with GPI-80 to support migration. Knockdown of either GPI-80 or ITGAM was sufficient to perturb undifferentiated HSPC in stroma co-culture. These findings indicate that human fetal HSC utilize common mechanisms with leukocytes for cell-cell interactions governing HSC self-renewal. We used microarrays to identify genes enriched in the CD90+ hematopoietic stem and progenitor population in fetal liver. RNA was extracted from enriched fetal liver hematopoietic stem and progenitor cells, and downstream progenitors, for comparison based on Affymetrix arrays.
2015-01-23 | E-GEOD-54314 | biostudies-arrayexpress