Etv2 rescues Flk1 mutant embryoid bodies.
Etv2 rescues Flk1 mutant embryoid bodies.
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Etv2 拯救 Flk1 突变胚状体。
DOI：
10.1002/dvg.22396
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Garry,DanielJ
中科院分区：
文献类型：
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作者：
Rasmussen,TaraL;Martin,CindyM;Walter,CamilleA;Shi,Xiaozhong;Perlingeiro,Rita;Koyano-Nakagawa,Naoko;Garry,DanielJ
Independent mouse knockouts ofEtv2andFlk1are embryonic lethal and lack hematopoietic and endothelial lineages. We previously reported that Flk1 activatesEtv2in the initiation of hematopoiesis and vasculogenesis. However,Flk1and its ligandVEGFare expressed throughout development, from E7.0 to adulthood, whereasEtv2is expressed only transiently during embryogenesis. These observations suggest a complex regulatory interaction between Flk1 and Etv2. To further examine the Flk1 and Etv2 regulatory interaction, we transducedEtv2andFlk1mutant ES cells with viral integrants that inducibly overexpress Flk1 or Etv2. We demonstrated that forced expression of Etv2 rescued the hematopoietic and endothelial potential of differentiatingFlk1andEtv2mutant cells. We further discovered that forced expression of Flk1 can rescue that of theFlk1, but notEtv2mutant cells. Therefore, we conclude that the requirement for Flk1 can be bypassed by expressing Etv2, supporting the notion that disruption of Etv2 expression is responsible for the early phenotypes of theEtv2andFlk1mutant embryos. genesis 51:471–480.© 2013 Wiley Periodicals, Inc.
