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Activation of lineage competence in hemogenic endothelium precedes the formation of hematopoietic stem cell heterogeneity

ABSTRACT: Activation of lineage competence in hemogenic endothelium precedes the formation of hematopoietic stem cell heterogeneity

PROVIDER: PRJNA773771 | ENA |

REPOSITORIES: ENA

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Activation of lineage competence in hemogenic endothelium precedes the formation of hematopoietic stem cell heterogeneity [Zebrafish.STRT-seq]

Project description:Activation of lineage competence in hemogenic endothelium precedes the formation of hematopoietic stem cell heterogeneity [Zebrafish.STRT-seq]

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Activation of lineage competence in hemogenic endothelium precedes the formation of hematopoietic stem cell heterogeneity [Zebrafish.scRNA-seq]

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Activation of lineage competence in hemogenic endothelium precedes the formation of hematopoietic stem cell heterogeneity

Project description:Using a combination of single-cell multi-omics, lineage tracing and functional assays, we show that embryonic HSPCs are originated from heterogeneous hemogenic endothelial cells (HECs) during zebrafish embryogenesis.

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Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [expression]

Project description:Scl/Tal1 confers hemogenic competence and prevents cardiomyogenesis in embryonic endothelium. Here we show that Scl both directly activates a broad gene regulatory network required for hematopoietic stem/progenitor cell (HS/PC) development, and represses transcriptional regulators required for cardiogenesis. Cardiac repression occurs during a short developmental window through Scl binding to distant cardiac enhancers that harbor H3K4me1 at this stage. Scl binding to hematopoietic regulators extends throughout HS/PC and erythroid development and spreads from distant enhancers to promoters. Surprisingly, Scl complex partners Gata 1 and 2 are dispensable for hematopoietic versus cardiac specification and Scl binding to the majority of its target genes. Nevertheless, Gata factors co-operate with Scl to activate selected transcription factors to facilitate HS/PC emergence from hemogenic endothelium. These results uncover a dual function for Scl in dictating hematopoietic versus cardiac fate choice and suggest a mechanism by which lineage-specific bHLH factors direct the divergence of competing fates. Examination of Scl target genes in ES cell derived day4 EB (embryoid body) Flk+ mesodermal cells

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