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• W2314156792 abstract "Endoglin (CD105) is an accessory receptor for TGF-beta signaling and is required for normal hemangioblast, early hematopoietic and vascular development. We have previously shown that an upstream enhancer, Eng-8, together with the promoter region, mediates robust endothelial expression in developing embryos and when coupled with two intronic enhancers, Eng +7 and Eng +9 also targets blood clusters in the dorsal aorta, fetal liver and placenta. The hemato-endothelial activity of this composite regulatory module was also shown to be dependent on Gata and Ets binding motifs. This current study was motivated by our desire to first, establish whether these enhancer modules cooperate to target the earliest blood precursors, i.e. hemangioblasts and hemogenic endothelial cells (HE) and second, to determine whether these regulatory elements could be used to enrich haemangioblasts and HE cells. To this end, we targeted various combinations of Eng promoter and wild-type and mutant enhancers with lacZ reporters into the HPRT loci of HM1 ES cells and evaluated the potential of Endoglin regulatory elements to target blast colony forming cells (BL-CFCs) and HEl cells. Our results showed that the -8/promoter/+7/+9 combination preferentially targeted BL-CFCs within the Flk1+ cell compartment in day 3 embryoid bodies in a Gata2 dependent manner. By contrast, the -8/P construct targeted cells with hematopoietic potential within Tie2 +, c-Kit + HE cells in day 2 liquid cultures. Importantly, these combinations of regulatory elements enrich these cell fractions when surface Endoglin alone proves inadequate. Utilising these elements as a gauge of the transcriptional milieu of hemangioblast and HE cell commitment, we have sorted cell fractions by flowcytometry and performed transcriptomic analysis to identify signaling pathways that are differentially active in these cells and identified and validated markers in vivo. Taken together, our results show that when different types of cells share expression of a gene but utilise distinct combinations of regulatory elements to express that gene, regulatory elements can be used to isolate and enrich cells when the gene itself lacks sufficient discriminative value. Endoglin (CD105) is an accessory receptor for TGF-beta signaling and is required for normal hemangioblast, early hematopoietic and vascular development. We have previously shown that an upstream enhancer, Eng-8, together with the promoter region, mediates robust endothelial expression in developing embryos and when coupled with two intronic enhancers, Eng +7 and Eng +9 also targets blood clusters in the dorsal aorta, fetal liver and placenta. The hemato-endothelial activity of this composite regulatory module was also shown to be dependent on Gata and Ets binding motifs. This current study was motivated by our desire to first, establish whether these enhancer modules cooperate to target the earliest blood precursors, i.e. hemangioblasts and hemogenic endothelial cells (HE) and second, to determine whether these regulatory elements could be used to enrich haemangioblasts and HE cells. To this end, we targeted various combinations of Eng promoter and wild-type and mutant enhancers with lacZ reporters into the HPRT loci of HM1 ES cells and evaluated the potential of Endoglin regulatory elements to target blast colony forming cells (BL-CFCs) and HEl cells. Our results showed that the -8/promoter/+7/+9 combination preferentially targeted BL-CFCs within the Flk1+ cell compartment in day 3 embryoid bodies in a Gata2 dependent manner. By contrast, the -8/P construct targeted cells with hematopoietic potential within Tie2 +, c-Kit + HE cells in day 2 liquid cultures. Importantly, these combinations of regulatory elements enrich these cell fractions when surface Endoglin alone proves inadequate. Utilising these elements as a gauge of the transcriptional milieu of hemangioblast and HE cell commitment, we have sorted cell fractions by flowcytometry and performed transcriptomic analysis to identify signaling pathways that are differentially active in these cells and identified and validated markers in vivo. Taken together, our results show that when different types of cells share expression of a gene but utilise distinct combinations of regulatory elements to express that gene, regulatory elements can be used to isolate and enrich cells when the gene itself lacks sufficient discriminative value." @default.
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• W2314156792 date "2013-08-01" @default.
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• W2314156792 title "Enriching hemangioblast and hemogenic endothelial cells using regulatory elements of the endoglin gene" @default.
• W2314156792 doi "https://doi.org/10.1016/j.exphem.2013.05.281" @default.
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