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dc.contributor.authorFleury, Maud
dc.contributor.authorEliades, Alexia
dc.contributor.authorCarlsson, P
dc.contributor.authorLacaud, Georges
dc.contributor.authorKouskoff, Valerie
dc.date.accessioned2015-10-02T11:43:37Zen
dc.date.available2015-10-02T11:43:37Zen
dc.date.issued2015-08-20en
dc.identifier.citationFOXF1 inhibits hematopoietic lineage commitment during early mesoderm specification. 2015: Developmenten
dc.identifier.issn1477-9129en
dc.identifier.pmid26293303en
dc.identifier.doi10.1242/dev.124685en
dc.identifier.urihttp://hdl.handle.net/10541/579031en
dc.description.abstractThe molecular mechanisms orchestrating early mesoderm specification are still poorly understood. In particular, how alternate cell fate decisions are regulated in nascent mesoderm remains mostly unknown. In the present study, we investigated both in vitro in differentiating embryonic stem cells and in vivo in gastrulating embryos the lineage specification of early mesodermal precursors expressing or not the Forkhead transcription factor FOXF1. Our data revealed that FOXF1-expressing mesoderm is derived from FLK1(+) progenitors and that in vitro this transcription factor is expressed in smooth muscle and transiently in endothelial lineages but not in hematopoietic cells. In gastrulating embryos, FOXF1 marks most extra-embryonic mesoderm derivatives including the chorion, the allantois, the amnion and a subset of endothelial cells. Similarly to the in vitro situation, FOXF1 expression is excluded from the blood islands and blood cells. Further analysis revealed an inverse correlation between hematopoietic potential and FOXF1 expression in vivo with increase commitment toward primitive erythropoiesis in Foxf1 deficient embryos while FOXF1-enforced expression in vitro was shown to repress hematopoiesis. Altogether our data establish that, during gastrulation, FOXF1 marks all posterior primitive streak extra-embryonic mesoderm derivatives with the remarkable exception of the blood lineage. Our study further suggests that this transcription factor is implicated in actively restraining the specification of mesodermal progenitors to hematopoiesis.
dc.languageENGen
dc.language.isoenen
dc.rightsArchived with thanks to Development (Cambridge, England)en
dc.titleFOXF1 inhibits hematopoietic lineage commitment during early mesoderm specification.en
dc.typeArticleen
dc.contributor.departmentCancer Research UK Stem Cell Hematopoiesis Group, Cancer Research UK Manchester Institute, The University of Manchester, Wilmslow Road, M20 4BX, UKen
dc.identifier.journalDevelopmenten
refterms.dateFOA2020-05-01T14:22:40Z
html.description.abstractThe molecular mechanisms orchestrating early mesoderm specification are still poorly understood. In particular, how alternate cell fate decisions are regulated in nascent mesoderm remains mostly unknown. In the present study, we investigated both in vitro in differentiating embryonic stem cells and in vivo in gastrulating embryos the lineage specification of early mesodermal precursors expressing or not the Forkhead transcription factor FOXF1. Our data revealed that FOXF1-expressing mesoderm is derived from FLK1(+) progenitors and that in vitro this transcription factor is expressed in smooth muscle and transiently in endothelial lineages but not in hematopoietic cells. In gastrulating embryos, FOXF1 marks most extra-embryonic mesoderm derivatives including the chorion, the allantois, the amnion and a subset of endothelial cells. Similarly to the in vitro situation, FOXF1 expression is excluded from the blood islands and blood cells. Further analysis revealed an inverse correlation between hematopoietic potential and FOXF1 expression in vivo with increase commitment toward primitive erythropoiesis in Foxf1 deficient embryos while FOXF1-enforced expression in vitro was shown to repress hematopoiesis. Altogether our data establish that, during gastrulation, FOXF1 marks all posterior primitive streak extra-embryonic mesoderm derivatives with the remarkable exception of the blood lineage. Our study further suggests that this transcription factor is implicated in actively restraining the specification of mesodermal progenitors to hematopoiesis.


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