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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Charles Girardot

PROVIDER: E-MTAB-12957 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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2014-11-14 | E-GEOD-51337 | 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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