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An erythroid-biased FOShi hematopoietic multipotent progenitor subpopulation contributes to adaptation to chronic hypoxia

ABSTRACT: An erythroid-biased FOShi hematopoietic multipotent progenitor subpopulation contributes to adaptation to chronic hypoxia

PROVIDER: PRJNA1160855 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30660919_1.fastq.gz	Fastqsanger.gz
	SRR30660919_2.fastq.gz	Fastqsanger.gz
	SRR30660920_1.fastq.gz	Fastqsanger.gz
	SRR30660920_2.fastq.gz	Fastqsanger.gz
	SRR30660921_1.fastq.gz	Fastqsanger.gz

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An erythroid-biased FOShi hematopoietic multipotent progenitor subpopulation contributes to adaptation to chronic hypoxia

Project description:Single-cell transcriptome analysis revealed an enrichment of Fos+ MPP subpopulations in mouse bone marrow under hypoxic conditions. To validate the biological characteristics and hypoxia stress response of the Fos+ MPP subpopulation, we used Fos-2A-tdTomato mice to establish a HAPC model. We then sorted Fos+ and Fos- MPP cells for low-input DNA methylation sequencing analysis.

2025-05-29 | GSE277134 | GEO

Nucleoporin Nup358 drives the differentiation of myeloid-biased multipotent progenitors by modulating HDAC3 nuclear translocation

Project description:We report that Nup358, a nucleoporin linked to acute myeloid leukemia and myeloproliferative neoplasms, is required for the developmental progression of early myeloid progenitors. We found that loss of Nup358 in mice is associated with the accumulation of myeloid-primed multipotent progenitors (MPPs) in bone marrow and the loss of myeloid-committed progenitors and mature myeloid cells. Accumulated MPPs in Nup358 knockout mice are greatly restricted to megakaryocyte/erythrocyte biased MPP2 cells and fail to progress into committed myeloid progenitors.

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Hemeatopoietic stem cells but not multipotent progenitors drive erythropoiesis during chronic erythroid stress in EPO transgenic mice

Project description:The hematopoietic stem cell (HSC) compartment consists of a small pool of cells capable of replenishing all blood cells. Although it is established that the hematopoietic system is assembled as a hierarchical organization under steady-state conditions, emerging evidence suggests that distinct differentiation pathways may exist in response to acute stress. However, it remains unclear how different hematopoietic stem and progenitor cell subpopulations behave under sustained chronic stress. Here, by using adult transgenic mice over-expressing erythropoietin (EPO; Tg6) and a combination of in vivo, in vitro, and deep sequencing approaches, we found that HSCs respond differentially to chronic erythroid stress than their closely related multipotent progenitors (MPPs). Specifically, HSCs exhibit a vastly committed erythroid progenitor profile with enhanced cell division, while MPPs display erythroid and myeloid cell signatures and an accumulation of uncommitted cells. Thus, our results identify HSCs as master regulators of chronic stress erythropoiesis, potentially circumventing the hierarchical differentiation-detour.

2018-05-11 | GSE113053 | GEO

Nucleoporin Nup358 drives the differentiation of myeloid-biased multipotent progenitors by modulating HDAC3 nuclear translocation

Project description:Nucleoporin Nup358 drives the differentiation of myeloid-biased multipotent progenitors by modulating HDAC3 nuclear translocation

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SCL and c-Kit controlled gene expression in erythroid progenitor cell line

Project description:SCL/TAL1, a tissue-specific transcription factor of the basic helix-loop-helix (bHLH) family, and c-Kit, a tyrosine kinase receptor, control hematopoietic stem cell survival and quiescence. Here we report that SCL and c-Kit signaling control a common gene expression signature, of which 19 genes are associated with apoptosis. In vivo, SCL levels are limiting for the clonal expansion of Kit+ multipotent and erythroid progenitors. In addition, increased SCL expression specifically enhances the sensitivity of multipotent and megakaryocyte/erythroid progenitors to Steel factor (KIT ligand), whilst a DNA binding mutant antagonizes KIT function and induces apoptosis in progenitors. We conclude that Scl operates downstream of Kit to support the survival of megakaryocyte/erythroid progenitors. Finally, higher SCL expression upregulates Kit in normal bone marrow cells and increases chimerism after bone marrow transplantation, indicating that Scl is also upstream of Kit. We conclude that Scl and Kit establish a positive feedback loop in multipotent and megakaryocyte/erythroid progenitors.

2013-07-06 | GSE48557 | GEO

SCL and c-Kit controlled gene expression in erythroid progenitor cell line

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Uncovering human yolk sac-derived innate lymphoid-biased multipotent progenitors prior to hematopoietic stem cell formation

Project description:Uncovering human yolk sac-derived innate lymphoid-biased multipotent progenitors prior to hematopoietic stem cell formation

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Hemeatopoietic stem cells but not multipotent progenitors drive erythropoiesis during chronic erythroid stress in EPO transgenic mice

Project description:Hemeatopoietic stem cells but not multipotent progenitors drive erythropoiesis during chronic erythroid stress in EPO transgenic mice

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Uncovering human yolk sac-derived innate lymphoid-biased multipotent progenitors prior to hematopoietic stem cell formation (scRNA-Seq)

Project description:Uncovering human yolk sac-derived innate lymphoid-biased multipotent progenitors prior to hematopoietic stem cell formation (scRNA-Seq)

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