Tracking spatio-temporal dynamics of the endothelial niche during fetal hematopoiesis
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PROVIDER: PRJNA954415 | ENA |
REPOSITORIES: ENA
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Project description:The emergence of the hematopoietic system occurs in temporal waves across different tissues during mouse development. During these waves, the endothelial niche serves as a source of hematopoietic cells and provides molecular cues that potentially shape the tissue-specific lineage output. Although the endothelial-to-hematopoietic transition in the aorta-gonad-mesonephros is well understood, a systematic analysis of hematopoietic progenitors and their endothelial niche across fetal tissues is lacking. Here, we leverage single-cell RNA-sequencing of micro-dissected fetal tissues during their peak of hematopoietic activity to systematically compare hematopoietic progenitors and the endothelial niche. We predict stage-specific interactions accompanying the transition of yolk sac endothelium to primitive and definitive hematopoietic fates and reveal distinct roles for fetal liver vascular niches. Furthermore, we provide in vitro evidence that lipid signaling by sphingosine-1-phosphate producing erythrocyte progenitors supports hematopoietic stem cell expansion in fetal liver. Our resource deciphers the temporal waves of hematopoietic development within distinct vascular niches.
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Project description:Adult hematopoietic stem cells (HSCs) reside primarily in bone marrow. However, hematopoietic stresses such as myelofibrosis, anemia, pregnancy, infection or myeloablation can mobilize HSCs to the spleen and induce extramedullary hematopoiesis (EMH). While the bone marrow HSC niche has been studied intensively, the EMH niche has received little attention. Here, we systematically assessed the physiological sources of the key niche factors, SCF and CXCL12, in the mouse spleen after EMH induction by cyclophosphamide plus granulocyte colony-stimulating factor, blood loss, or pregnancy. In each case, Scf was expressed by endothelial cells and Tcf21+ stromal cells, primarily around sinusoids in red pulp, while Cxcl12 was expressed by a subset of Tcf21+ stromal cells. EMH induction markedly expanded the Scf-expressing endothelial cells and stromal cells by inducing proliferation. Most splenic HSCs were adjacent to Tcf21+ stromal cells in red pulp. Conditional deletion of Scf from spleen endothelial cells or Scf or Cxcl12 from Tcf21+ stromal cells severely reduced spleen EMH and reduced blood cell counts without affecting bone marrow hematopoiesis. Endothelial cells and Tcf21+ stromal cells thus create the splenic EMH niche, which is necessary for the physiological response to diverse hematopoietic stresses. Unfractionated spleen cells (2 replicates) and FACS-sorted VE-cadherein negative Scf-GFP positive cells (3 replicates)
2015-08-01 | E-GEOD-71288 | biostudies-arrayexpress
Project description:Adult hematopoietic stem cells (HSCs) reside primarily in bone marrow. However, hematopoietic stresses such as myelofibrosis, anemia, pregnancy, infection or myeloablation can mobilize HSCs to the spleen and induce extramedullary hematopoiesis (EMH). While the bone marrow HSC niche has been studied intensively, the EMH niche has received little attention. Here, we systematically assessed the physiological sources of the key niche factors, SCF and CXCL12, in the mouse spleen after EMH induction by cyclophosphamide plus granulocyte colony-stimulating factor, blood loss, or pregnancy. In each case, Scf was expressed by endothelial cells and Tcf21+ stromal cells, primarily around sinusoids in red pulp, while Cxcl12 was expressed by a subset of Tcf21+ stromal cells. EMH induction markedly expanded the Scf-expressing endothelial cells and stromal cells by inducing proliferation. Most splenic HSCs were adjacent to Tcf21+ stromal cells in red pulp. Conditional deletion of Scf from spleen endothelial cells or Scf or Cxcl12 from Tcf21+ stromal cells severely reduced spleen EMH and reduced blood cell counts without affecting bone marrow hematopoiesis. Endothelial cells and Tcf21+ stromal cells thus create the splenic EMH niche, which is necessary for the physiological response to diverse hematopoietic stresses.
2015-08-01 | GSE71288 | GEO
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2020-12-07 | GSE158849 | GEO
Project description:Proper control of inflammatory responses is essential for embryonic development, but the underlying mechanism is poorly understood. Here, we show that under physiological conditions, inactivation of ISG15, an inflammation amplifier, is associated with the interaction of Beclin 1 (Becn1), via its ECD domain, with STAT3 in the major fetal hematopoietic organ of mice. Conditional loss of Becn1 caused sequential dysfunction and exhaustion of fetal liver hematopoietic stem cells, leading to lethal inflammatory cell-biased hematopoiesis in the fetus. Molecularly, the absence of Becn1 resulted in the release of STAT3 from Becn1 tethering and subsequent phosphorylation and translocation to the nucleus, which in turn directly activated the transcription of ISG15 in fetal liver hematopoietic cells, coupled with increased ISGylation and production of inflammatory cytokines, whereas inactivating STAT3 reduced ISG15 transcription and inflammation but improved hematopoiesis potential, and further silencing ISG15 mitigated the above collapse in the Becn1 null hematopoietic lineage. The Becn1-STAT3-ISG15 axis remains functional in Atg5/7-disrupted fetal hematopoietic organs. These results suggest that Becn1, in an autophagy-independent manner, secures hematopoiesis and survival of the fetus by directly inhibiting STAT3-ISG15 activation to prevent cytokine storms. Our findings highlight a previously undocumented role of Becn1 in governing ISG15 to safeguard the fetus.
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Project description:Modelling ecological niches of migratory animals requires incorporating a temporal dimension, in addition to space. Here, we introduce an approach to model multigenerational migratory insects using time-partitioned environmental variables (by months and years) and time- and behaviour-partitioned records (breeding records to model reproductive habitat). We apply this methodology to modelling the Palearctic-African migratory cycle of the Painted Lady butterfly (Vanessa cardui), based on data encompassing 36 years (646 breeding sites from 30 countries). Each breeding record is linked to a particular time (month and year), and the associated values of the bioclimatic variables are used for an ensemble modelling strategy, to finally obtain monthly projections. The results show obligated movements, mostly latitudinal, for the species' successive generations across the overall range, and only scattered locations show high probabilities of reproduction year-round. The southernmost reproductive areas estimated for the Palearctic-African migratory pool reach equatorial latitudes from December to February. We thus propose a potential distribution for the winter 'missing generations' that would expand the V. cardui migration cycle to encompass about 15 000 km in latitude, from northernmost Europe to equatorial Africa. In summer, Europe represents the major temporary resource for V. cardui, while January and February show the lowest overall suitability values, and they are potentially the most vulnerable period for the species to suffer yearly bottlenecks. In summary, we demonstrate the potential of the proposed niche modelling strategy to investigate migratory movements of insects.
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