Combinatorial effects of Flk1 and Tal1 on vascular and hematopoietic development in the mouse.
作者： Masatsugu Ema , Patrick Faloon , Wen Jie Zhang , Masanori Hirashima , Tammy Reid
DOI: 10.1101/GAD.1049803
关键词:
摘要: Mouse embryos mutant for the VEGF receptor, VEGFR2, Flk-1, or Kdr, fail to form both endothelial and hematopoietic cells, suggesting a possible role in common progenitor lineages. The transcription factor Tal1 (Scl), is not expressed Flk1 −/− embryos, consistent with downstream pathway. We tested whether expression of under promoter was sufficient rescue loss cells mutants. Only partial hematopoiesis development observed vivo. However, −/Tal1 embryonic stem (ES) were capable blast colony formation vitro at levels equivalent +/− heterozygotes. Ectopic mouse ES caused no obvious pathology but increased number forming (BL-CFCs) enhanced their potential. These single-cell-derived BL-CFCs also produced smooth muscle vitro. Increased inhibited differentiation this assay, whereas promoted formation. propose model which combinatorial effects act regulate cell fate choice early into hematopoietic, endothelial,
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