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Transcription factor Hoxb5 reprograms B cells into functional T lymphocytes [RNA-Seq]

ABSTRACT: Natural hematopoietic stem cells are currently the only cell resource to generate entire T lymphopoiesis in vivo. Altenatively, functional and non-tumorigenic T lymphocytes converted from the other cell types remain unsuccessful. Evidence is still lacking about the concept that 'lineage-switching factors' (LSFs) exist in HSC, whose re-activation in progeny cells can accomplish lineage conversions. Here we show that upon ectopic expression of Hoxb5(a HSC-specific transcription factor), the Pro-/Pre-B cells were induced into functional early T cell progenitors(iETPs) in vivo. The reprogramming process initiated in the bone marrow and accomplished in the thymus at ETP stage. Strikingly, the T lymphocytes derived from iETPs resemble their natural counterparts in transcriptome pattern, hierarchical differentiation, tissue distribution and immune functions. Our observations pave the way for achieving lineage regeneration by direct reprogramming autologous somatic cells in vivo. Further, our success in haematopoietic system may build a paradigm for LSF-mediated regeneration of other tissues.

ORGANISM(S): Mus musculus

PROVIDER: GSE93107 | GEO | 2018/02/07

REPOSITORIES: GEO

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Neogenin-1 distinguishes between myeloid-biased and balanced Hoxb5+ mouse long-term hematopoietic stem cells

Project description:Hematopoietic stem cells (HSCs) self-renew and generate all blood cells. Recent studies with single-cell transplants and lineage tracing suggest that adult HSCs are diverse in their reconstitution and lineage potentials. However, prospective isolation of these subpopulations has remained challenging. Here, we identify Neogenin-1 (NEO1) as a unique surface marker on a fraction of mouse HSCs labeled with Hoxb5, a specific reporter of long-term HSCs (LT-HSCs). We show that NEO1+Hoxb5+ LT-HSCs expand with age and respond to myeloablative stress in young mice, while NEO1–Hoxb5+ LT-HSCs exhibit no significant change in number. Furthermore, NEO1+Hoxb5+ LT-HSCs are more often in the G2/S cell cycle phase compared to NEO1–Hoxb5+ LT-HSCs in both young and old bone marrow. Upon serial transplantation, NEO1+Hoxb5+ LT-HSCs exhibit myeloid-biased differentiation and reduced reconstitution, while NEO1–Hoxb5+ LT-HSCs are lineage-balanced and stably reconstitute recipients. Gene expression analysis reveals erythroid and myeloid priming in the NEO1+ fraction and association of quiescence and self-renewal-related transcription factors with NEO1− LT-HSCs. Finally, transplanted NEO1+Hoxb5+ LT-HSCs rarely generate NEO1–Hoxb5+ LT-HSCs, while NEO1–Hoxb5+ LT-HSCs repopulate both LT-HSC fractions. This supports a model in which dormant, balanced, NEO1–Hoxb5+ LT-HSCs can hierarchically precede active, myeloid-biased NEO1+Hoxb5+ LT-HSCs.

2019-11-10 | GSE130504 | GEO

Hoxb5 reprograms murine multipotent blood progenitors into hematopoietic stem cell-like cells

Project description:We performed the single cell RNA-seq for the Hoxb5 Mac-1+CD48+ SK cells, bone marrow HSC, bone marrow MPP, and fetal liver HSC by Smart-Seq2.

2022-06-30 | GSE183800 | GEO

Transcription factor Hoxb5 reprograms B cells into functional T lymphocytes

Project description:Transcription factor Hoxb5 reprograms B cells into functional T lymphocytes

| PRJNA414529 | ENA

Transcription factor Hoxb5 reprograms B cells into functional T lymphocytes [ChIP-Seq]

Project description:Chipseq were performed to analyze the targets of Hoxb5 in pro-/pre-B by over expression.

2018-02-07 | GSE105007 | GEO

Transcription factor Hoxb5 reprograms B cells into functional T lymphocytes [RNA-seq2]

Project description:Here we were performed RNAseq to analyze the transcriptome changing of Hoxb5 in Pro/pre-B by over expression.

2018-02-07 | GSE105768 | GEO

Transcription factor Hoxb5 reprograms B cells into functional T lymphocytes [RNA-seq2]

Project description:Transcription factor Hoxb5 reprograms B cells into functional T lymphocytes [RNA-seq2]

| PRJNA415304 | ENA

Transcription factor Hoxb5 reprograms B cells into functional T lymphocytes [ChIP-Seq]

Project description:Transcription factor Hoxb5 reprograms B cells into functional T lymphocytes [ChIP-Seq]

| PRJNA414411 | ENA

Macrophages trigger injury-induced hepatocyte reprogramming via IL-6/gp130/STAT3 axis [RNA-Seq]

Project description:The liver is a pivotal organ possessing remarkable regenerative capacity. By employing murine liver injury models and lineage tracing strategy, recent studies have demonstrated that differentiated hepatocytes undergo reprogramming to SOX9+HNF4α+ liver progenitor-like cells (LPLCs), and serve as a totally new cell source for mammalian liver regeneration. However, it is largely unknown how hepatocyte reprogramming is regulated. In this study, we focus on analyzing the microenvironment cues in triggering hepatocyte reprogramming in liver injuries. By performing single-cell RNA sequencing (scRNA-seq) of hepatocyte reprogramming in liver injury, we find immune response is significantly activated. Notably, by lineage depletion, macrophages, especially kupffer cells, but not T cells, B cells, natural killer cells or neutrophils, are found essential for hepatocyte reprogramming and liver regeneration. IL-6, derived specifically from activated kupffer cells, triggers hepatocyte reprogramming via gp130/STAT3 signaling. Furthermore, STAT3 triggers gene expression by binding to Arid1a-dependent pre-opened regeneration-responsive enhancers (RREs) of reprogramming genes. Collectively, this study provides key insights into kupffer cells/IL-6/STAT3-mediated hepatocyte reprogramming and liver regeneration, which may serve as the base for new therapeutic strategies in facilitating endogenous repair mechanisms.

2022-08-24 | GSE193849 | GEO

Macrophages trigger injury-induced hepatocyte reprogramming via IL-6/gp130/STAT3 axis [ChIP-Seq]

2022-08-24 | GSE193848 | GEO

OSKM-induced epithelial cells of mouse intestine [scRNA-seq]

Project description:Tissue regeneration after injury is thought to involve the dedifferentiation of somatic cells, which is often understood as evidence for natural adaptative reprogramming in vivo. In the intestinal epithelium, acute tissue damage triggers the rapid emergence of injury-responsive cells with fetal-like characteristics, a sign of dedifferentiation. However, there is no direct evidence that tissue regeneration involves a shared molecular mechanism with direct cellular reprogramming. It is also not known whether dedifferentiation shares a single (de)differentiation pathway or consists of multiple parallel routes between adult and fetal states. Here, we induced dedifferentiation of intestinal epithelial cells by forced partial reprogramming in vivo using the “Yamanaka factors” (Oct4, Sox2, Klf4 and c-Myc: OSKM). The induced dedifferentiation showed shared molecular features of intestinal regeneration, with rapid transition from homeostatic intestinal cell types to injury-responsive-like cells sharing a common gene signature of revival stem cells and atrophy-induced villus epithelial cells. When applied to intestinal organoids, induced dedifferentiation allowed the organoids to adopt fetal characteristics ex vivo, suggesting a direct effect on the intestinal epithelium. In vivo, induced dedifferentiation promoted regeneration from acute tissue injury caused by ionizing radiation (IR) via the formation of injury-responsive-like cells. Taken together, in the intestinal epithelium, in vivo reprogramming shares the same molecular pathway as damage-induced tissue regeneration and facilitates the repair process.

2023-11-26 | GSE237173 | GEO

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