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Inferring rules of lineage commitment in haematopoiesis

ABSTRACT: Fractionation of EML cells isolated based on surface expression of immunophenotypic markers reveals the existence of a subpopulation that has undergone spontaneous commitment to an erythroid fate. Uncommitted fractions were compared to committed cells, derived from both spontaneous (EryCP) and cytokine-driven (Ediff) commitment.

ORGANISM(S): Mus musculus

PROVIDER: GSE34605 | GEO | 2012/02/14

SECONDARY ACCESSION(S): PRJNA150471

REPOSITORIES: GEO

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Inferring rules of lineage commitment in haematopoiesis

Project description:Fractionation of EML cells isolated based on surface expression of immunophenotypic markers reveals the existence of a subpopulation that has undergone spontaneous commitment to an erythroid fate. Uncommitted fractions were compared to committed cells, derived from both spontaneous (EryCP) and cytokine-driven (Ediff) commitment. EML cells were separated by flow cytometry based on their expression of the markers Sca1, CD34 and cKit as described.

2012-02-14 | E-GEOD-34605 | biostudies-arrayexpress

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A lineage commitment checkpoint in early ILC development [single cell RNA-seq]

Project description:Understanding how cellular function is imprinted during development requires the identification of factors controlling lineage specification and commitment, and the intermediate progenitors in which they act. Using population level and single cell approaches, we examine transcriptional and functional heterogeneity within early innate lymphoid cells (ILC) progenitors. We identify a developmental bifurcation toward dendritic cell fate that reveals the uncommitted state of early specified ILC progenitors. We subsequently characterize an ILC-commitment checkpoint controlled by the transcription factor TCF-1. The present study reveals unexpected heterogeneity within early innate progenitor populations, and characterizes lineage infidelity that accompanies early ILC specification prior to commitment.

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Cancer-associated ASXL1 mutations may act as gain-of-function mutations of the ASXL1-BAP1 complex

Project description:ASXL1 is the obligate regulatory subunit of a deubiquitinase complex whose catalytic subunit is BAP1. Heterozygous mutations of ASXL1 that result in premature truncations are frequent in myeloid leukemias and Bohring-Opitz syndrome. Here, we demonstrate that truncated ASXL1 proteins confer enhanced activity on the ASXL1-BAP1 complex. Stable expression of truncated, hyperactive ASXL1-BAP1 complexes in a hematopoietic precursor cell line resulted in global erasure of H2AK119Ub, striking depletion of H3K27me3, selective upregulation of a subset of genes whose promoters bore both H2AK119Ub and H3K4me3, and spontaneous differentiation to the mast cell lineage. These outcomes required the catalytic activity of BAP1, indicating these events were downstream consequences of H2AK119Ub erasure. In bone marrow precursors, truncated ASXL1-BAP1 expression cooperated with TET2 loss-of-function to increase differentiation to the myeloid lineage in vivo. We propose that pathological ASXL1 mutations confer gain-of-function on the ASXL-BAP1 complex. ChIP-Seq for H2AK119Ub, H3K4me3, H3K27me3 on EML cells. RNA-Seq on EML cells expressing ASXL1(1-479)+BAP1 and control.

2015-03-11 | E-GEOD-65555 | biostudies-arrayexpress

Downstream Targets of HOXB4 in the primitive hematopoietic progenitor EML Cell line

2010-04-20 | GSE20604 | GEO

Downstream Targets of HOXB4 in the primitive hematopoietic progenitor EML Cell line

Project description:Enforced expression of the homeobox transcription factor HOXB4 has been shown to enhance hematopoietic stem cell (HSC) self-renewal and expansion ex vivo and in vivo. In order to investigate the largely unknown downstream targets of HOXB4 in hematopoietic progenitor cells, HOXB4 was constitutively overexpressed in the primitive hematopoietic progenitor cell line, EML. Gene expression differences were compared between KLS (c-Kit+, Lin-, Sca-1+)-EML cells that overexpressed HOXB4 (KLS-EML-HOXB4) to control KLS-EML cells that were transduced with vector alone. ChIP-chip was used to identify promoter regions bound by HOXB4. We overexpressed HOXB4 in EML cells. We isolated 3 separate single cell clones as assessed by Southern Blot Analysis (3 clones for EML-HOXB4 and 3 clones for control EML-GFP cells). RNA was isolated from the KLS (c-Kit+, Lin-, Sca-1+) fraction of each single cell clone population and processed for hybridization to array chips using established lab protocols. Chip-Chip analysis of the three HOXB4 overexpressing clones was performed to identify HOXB4 bound promoters.

2010-04-20 | E-GEOD-20604 | biostudies-arrayexpress

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