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Reprogramming Mouse Fibroblasts into Engraftable Myeloerythroid and Lymphoid Progenitors: Induction and Underlying Mechanisms (ChIP-Seq)

ABSTRACT: Here we show that hematopoietic transcription factors Scl, Lmo2, Runx1 and Bmi1 can convert a developmentally-distant lineage (fibroblasts) into “induced hematopoietic progenitors” (iHPs). We analyzed transcriptomic data for cell undergoing the transdifferentiation process at several time-points of the process.

ORGANISM(S): Mus musculus

PROVIDER: GSE86197 | GEO | 2016/09/30

SECONDARY ACCESSION(S): PRJNA340870

REPOSITORIES: GEO

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Reprogramming Mouse Fibroblasts into Engraftable Myeloerythroid and Lymphoid Progenitors: Induction and Underlying Mechanisms (BeadChip)

Project description:Here we show that hematopoietic transcription factors Scl, Lmo2, Runx1 and Bmi1 can convert a developmentally-distant lineage (fibroblasts) into “induced hematopoietic progenitors” (iHPs). We analyzed transcriptomic data for cell undergoing the transdifferentiation process at several time-points of the process.

2016-09-30 | GSE86196 | GEO

Reprogramming mouse fibroblasts into engraftable myeloerythroid and lymphoid progenitors.

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Effect of endoglin loss on embryoid bodies

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ATAC-seq of mouse Embryonic Stem Cell (mESC) line-derived cells subjected or not to doxycycline (dox)-induced overexpression of transcription factors

Project description:The ATAC-seq is one of three readouts of an experiment carried out to assess the ability of different combinations of hematopoietic transcription factors to elicit the transdifferentiation of a mESC-derived non-hematopoietic cell type (vascular smooth muscle cells) into hematopoietic precursors upon dox-induced overexpression. The assessed trascription factors are Tal1, Lyl1 and Lmo2 (i3TFs), Runx1, Cbfb, Gata2, Fli1, Erg (i5TFs) and Runx1, Cbfb, Gata2, Tal1, Fli1, Lyl1, Erg, Lmo2 (i8TFs). The constructs for TF expression were stably integrated into mESCs and their expression induced by treatment with dox. i: inducible.

2023-05-08 | E-MTAB-12955 | biostudies-arrayexpress

RNA-seq of mouse Embryonic Stem Cell (mESC) line-derived cells subjected or not to doxycycline (dox)-induced overexpression of transcription factors (TFs)

Project description:The RNA-seq is one of three readouts of an experiment carried out to assess the ability of different combinations of hematopoietic transcription factors to elicit the transdifferentiation of a mESC-derived non-hematopoietic cell type (vascular smooth muscle cells) into hematopoietic precursors upon dox-induced overexpression. The assessed trascription factors are Tal1, Lyl1 and Lmo2 (i3TFs), Runx1, Cbfb, Gata2, Fli1, Erg (i5TFs) and Runx1, Cbfb, Gata2, Tal1, Fli1, Lyl1, Erg, Lmo2 (i8TFs). The constructs for TF expression were stably integrated into mESCs and their expression induced by treatment with dox. i: inducible.

2023-05-15 | E-MTAB-12957 | biostudies-arrayexpress

Reprogramming Mouse Fibroblasts into Engraftable Myeloerythroid and Lymphoid Progenitors: Induction and Underlying Mechanisms

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-09-30 | GSE86198 | GEO

Effect of endoglin loss on embryoid bodies

Project description:Analysis of embryonic sten cell-derived embryoid bodies following endoglin knock out. Loss of endoglin leads to profound reduction of key hematopoietic regulators including SCL, LMO2, Gata2, and TGF-? signaling molecule ALK-1. Results provide insight into molecular mechanisms underlying hemangioblast and primitive hematopoietic development. Total RNA obtained from differentiated day 3 EBs of endoglin knock out ES cells were compared to wild type E14 control ES cells.

2011-05-16 | E-GEOD-29300 | biostudies-arrayexpress

Divergent functions of hematopoietic transcription factors in lineage priming and differentiation during erythro-megakaryopoiesis

Project description:Combinatorial actions of relatively few transcription factors control hematopoietic differentiation. To investigate this process in erythro-megakaryopoiesis, we correlated the genome-wide chromatin occupancy signatures of four master hematopoietic transcription factors (GATA1, GATA2, SCL/TAL1 and FLI1) and three diagnostic histone modification marks with the gene expression changes that occur during development of primary megakaryocytes (MEG) and erythroblasts (ERY) from murine fetal liver hematopoietic stem/progenitor cells. We identified a robust, genome-wide mechanism of MEG-specific lineage priming by a previously described stem/progenitor cell-expressed transcription factor heptad (GATA2, LYL1, SCL/TAL1, FLI1, ERG, RUNX1, LMO2) binding to MEG-specific cis-regulatory modules in multipotential hematopoietic progenitors. This is followed by genome-wide GATA factor switching that mediates further induction of MEG-specific genes following lineage commitment. Interaction between GATA and ETS factors appears to be a key determinant of these processes. In contrast, ERY-specific lineage priming occurs is biased toward GATA2-independent mechanisms. In addition to its role in MEG lineage priming, GATA2 plays an extensive role in late megakaryopoiesis as a transcriptional repressor at loci defined by a specific DNA signature. Our findings reveal important new insights into how ERY and MEG lineages arise from a common bipotential precursor via overlapping and divergent functions of shared hematopoietic transcription factors. Gene expression changes during the development of primary megakaryocytes (MEG) and erythroblasts (ERY) from murine fetal liver hematopoietic stem/progenitor cells

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Divergent functions of hematopoietic transcription factors in lineage priming and differentiation during erythro-megakaryopoiesis

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Gene expression of human chord blood hematopoietic progenitor cells and induced hemato-endothelial progenitor cells derived from human iPSC

Project description:Induced pluripotent stem cells (iPSC) offer a promising platform to model early embryonic developmental processes, to create disease models and proof-of-concept experiments for regenerative medicine. However, generation of iPSC derived hemato-endothelial and hematopoietic progenitor cells for these applications is challenging due to variable and limited cell numbers, which necessitates enormous up-scaling or development of demanding protocols. Here, we unravel the function of key transcriptional regulators SCL, LMO2, GATA2, ETV2 (SLGE) on early hemato-endothelial specification and establish a fully inducible and stepwise hemato-endothelial forward programming system, based on SLGE regulated overexpression. Regulated induction of SLGE in stable SLGE-iPSC lines drives very efficient generation of large numbers of hemato-endothelial progenitor cells (HEP) (CD144+/CD73-), which generate hematopoietic progenitor cells (CD45+/CD34+/CD38-/CD45RA-/CD90+/CD49f+) through a gradual process of endothelial-to-hematopoietic transition (EHT).

2019-11-13 | GSE140221 | GEO

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