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Meis1 establishes the pre-hemogenic endothelial state prior to Runx1 expression [CITE-seq]

ABSTRACT: Meis1 establishes the pre-hemogenic endothelial state prior to Runx1 expression [CITE-seq]

PROVIDER: PRJNA809477 | ENA |

REPOSITORIES: ENA

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Meis1 establishes the pre-hemogenic endothelial state prior to Runx1 expression [CITE-seq]

Project description:Hematopoietic stem and progenitor cells (HSPCs) originate from an endothelial-to-hematopoietic transition (EHT) during embryogenesis. Characterization of early hemogenic endothelial (HE) cells is required to understand what drives hemogenic specification and to accurately define cells capable of undergoing EHT. Using Cellular Indexing of Transcriptomes and Epitopes by Sequencing (CITE-seq), we defined the early subpopulation of pre-HE cells based on both surface markers and transcriptomes. We identified the transcription factor Meis1 as an essential regulator of hemogenic cell specification in the embryo prior to Runx1 expression. Meis1 is expressed at the earliest stages of EHT and distinguishes pre-HE cells primed towards the hemogenic trajectory from the arterial endothelial cells that continue towards a vascular fate. Endothelial-specific deletion of Meis1 impaired the formation of functional Runx1-expressing HE which significantly impeded the emergence of pre-HSPC via EHT. Our findings implicate Meis1 in a critical fate-determining step for establishing EHT potential in endothelial cells.

2023-02-22 | GSE197244 | GEO

Meis1 establishes the pre-hemogenic endothelial state prior to Runx1 expression

2023-02-02 | GSE196047 | GEO

Meis1 establishes the pre-hemogenic endothelial state prior to Runx1 expression II

2023-02-22 | GSE197400 | GEO

Meis1 establishes the pre-hemogenic endothelial state prior to Runx1 expression

Project description:Meis1 establishes the pre-hemogenic endothelial state prior to Runx1 expression

| PRJNA803157 | ENA

Meis1 establishes the pre-hemogenic endothelial state prior to Runx1 expression II

Project description:Meis1 establishes the pre-hemogenic endothelial state prior to Runx1 expression II

| PRJNA810085 | ENA

Meis1 as an essential regulator of hemogenic cell specification in the embryo prior to Runx1 expression

Project description:Meis1 as an essential regulator of hemogenic cell specification in the embryo prior to Runx1 expression

| PRJEB52790 | ENA

Meis1 genomics

Project description:Meis1 function in leukemogenesis

| PRJEB50012 | ENA

Gene expression profiles upon Meis1 knockout in Hoxa9/Meis1-induced AML

Project description:Meis1 is found cooperatively activated with Hoxa7/a9 in AML, and it indeed promotes leukemogenic activities of Hoxa9. It is important to identify downstream target genes of Meis1 to understand its cooperative activity with Hoxa9 in leukemogenesis. We used microarrays to detail the global programme of gene expression upon Meis1 knockout. Murine primary bone marrow cells of the Rosa26-Cre-ERT2 knock-in mouse were transformed by retroviral transduction of Hoxa9 and floxed Meis1. The immortalized bone marrow cells were treated with 2 μM of 4-hydroxytamoxifen to delete Meis1 cDNA. Gene expression profiles were compared between the original Hoxa9/Meis1-expressing cells and Meis1 deleted (Hoxa9 only) cells.

2015-01-01 | E-GEOD-50645 | biostudies-arrayexpress

Gene expression profiles upon Meis1 knockout in Hoxa9/Meis1-induced AML

2015-01-01 | GSE50645 | GEO

Hoxa9 and Meis1 cooperatively induce addiction to Syk signaling by suppressing miR-146a in acute myeloid leukemia

Project description:The transcription factor Meis1 drives myeloid leukemogenesis in the context of Hox gene overexpression but is currently considered undruggable. We therefore investigated whether myeloid progenitor cells transformed by Hoxa9 and Meis1 become addicted to targetable signaling pathways. A comprehensive (phospho)proteomic analysis revealed that Meis1 increased Syk protein expression and activity. Syk upregulation occurs through a Meis1-dependent feed-forward loop. By dissecting this loop, we show that Syk is a direct target of miR-146a, whose expression is indirectly regulated by Meis1 through the transcription factor PU.1. In the context of Hoxa9 overexpression, Syk induces Meis1, recapitulating several leukemogenic features of Hoxa9/Meis1-driven leukemia. Finally, we show that Syk inhibition disrupts the identified regulatory loop, prolonging survival of mice with Hoxa9/Meis1-driven leukemia.

2017-06-14 | PXD004192 | Pride

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