Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA349470 | ENA |
REPOSITORIES: ENA
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Project description:FoxM1 is essential for quiescence and maintenance of hematopoietic stem cell
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2020-10-22 | GSE144712 | GEO
Project description:Adult and fetal hematopoietic stem cells (HSCs) display a glycolytic phenotype, which is required for maintenance of stemness; however, whether mitochondrial respiration is required to maintain HSC function is not known. Here we report that loss of the mitochondrial complex III subunit Rieske iron sulfur protein (RISP) in fetal mouse HSCs allows them to proliferate but impairs their differentiation, resulting in anemia and prenatal death. RISP null fetal HSCs displayed impaired respiration resulting in a decreased NAD+/NADH ratio. RISP null fetal HSCs and progenitors exhibited an increase in both DNA and histone methylation concomitant with increases in 2-hydroxyglutarate (2-HG), a metabolite known to inhibit DNA and histone demethylases. RISP inactivation in adult HSCs also impaired respiration resulting in loss of quiescence resulting in severe pancytopenia and lethality. Thus, respiration is dispensable for adult or fetal HSC proliferation, but essential for fetal HSC differentiation and maintenance of adult HSC quiescence.
2017-09-13 | PXD006054 | Pride
Project description:LIM domain binding protein 1 regulates a transcriptional program essential for hematopoietic stem cell maintenance
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Project description:C/EBPa controls acquisition and maintenance of adult hematopoietic stem cell quiescence
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Project description:Hematopoiesis is a series of lineage differentiation programs initiated from hematopoietic stem cells (HSCs) in the bone marrow (BM). To maintain lifelong hematopoiesis, the pool of HSCs is precisely maintained by diverse molecular mechanisms. CCCTC-binding factor (CTCF) is a DNA-binding zinc-finger protein which regulates its target gene expression by organizing higher order chromatin structures. Currently, the role for CTCF in controlling HSC homeostasis is unknown. By using a tamoxifen-induced CTCF conditional knockout mouse system, we demonstrate that CTCF is a critical regulator for the homeostatic maintenance of adult HSCs by retaining HSC cell cycle quiescence. Acute systemic CTCF ablation leads to a severe BM failure and rapid shrinkage of multiple c-Kithi progenitor populations, including Sca-1+ HSCs in adult mice. Similarly, a hematopoietic system-confined CTCF depletion elicits an acute loss of HSCs and highly increased mortality. Mixed BM chimeras reconstituted together with the supporting BM reveal that CTCF deficiency-mediated HSC depletion is a cell-autonomous effect. Although c-Kithi myeloid progenitors were severely reduced after ablating Ctcf gene, c-Kitint common lymphoid progenitors and their progenies were less affected by the lack of CTCF. Whole transcriptome analyses show that CTCF deficiency results in an enhanced expression of the cell cycle-promoting program and CTCF-depleted HSCs express higher level of reactive oxygen species (ROS). Importantly, in vivo treatment with the antioxidant partially rescued the c-Kithi population and their quiescence. We conclude that CTCF is a pivotal player in maintaining adult HSC pool likely through regulating ROS-dependent HSC quiescence. We used gene expression microarray to elucidate CTCF-regulated gene profiles of the Lin−Sca-1+c-Kithi (LSKs) stem/progenitor populations.
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Project description:Quiescence is essential for the long term maintenance of adult stem cells and tissue homeostasis. However, how stem cells maintain quiescence is still poorly understood. Here we show that stem cells in the dentate gyrus of the adult hippocampus actively transcribe the proactivation factor Ascl1 regardless of their activation state. We found that the inhibitor of DNA binding protein Id4 suppresses Ascl1 activity in neural stem cell cultures. Id4 sequesters Ascl1 heterodimerisation partner, promoting the degradation of Ascl1 protein and neural stem cell quiescence. Accordingly, elimination of Id4 from stem cells in the adult hippocampus results in abnormal accumulation of Ascl1 protein and premature stem cell activation. We also found that multiple signalling pathways converge on the regulation of Id4 to control the activity of hippocampal stem cells. Id4 therefore maintains quiescence of adult neural stem cells, in sharp contrast with its role of promoting the proliferation of embryonic neural progenitors.
2019-10-18 | GSE116997 | GEO