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由ETS转录因子ER71/ETV2精心编排的造血和内皮细胞程序的诱导。

Induction of hematopoietic and endothelial cell program orchestrated by ETS transcription factor ER71/ETV2.

作者信息

Liu Fang, Li Daofeng, Yu Yik Yeung Lawrence, Kang Inyoung, Cha Min-Ji, Kim Ju Young, Park Changwon, Watson Dennis K, Wang Ting, Choi Kyunghee

机构信息

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, USA.

Department of Genetics, Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, MO, USA.

出版信息

EMBO Rep. 2015 May;16(5):654-69. doi: 10.15252/embr.201439939. Epub 2015 Mar 23.

Abstract

The ETS factor ETV2 (aka ER71) is essential for the generation of the blood and vascular system, as ETV2 deficiency leads to a complete block in blood and endothelial cell formation and embryonic lethality in the mouse. However, the ETV2-mediated gene regulatory network and signaling governing hematopoietic and endothelial cell development are poorly understood. Here, we map ETV2 global binding sites and carry out in vitro differentiation of embryonic stem cells, and germ line and conditional knockout mouse studies to uncover mechanisms involved in the hemangiogenic fate commitment from mesoderm. We show that ETV2 binds to enhancers that specify hematopoietic and endothelial cell lineages. We find that the hemangiogenic progenitor population in the developing embryo can be identified as FLK1(high)PDGFRα(-). Notably, these hemangiogenic progenitors are exclusively sensitive to ETV2-dependent FLK1 signaling. Importantly, ETV2 turns on other Ets genes, thereby establishing an ETS hierarchy. Consequently, the hematopoietic and endothelial cell program initiated by ETV2 is maintained partly by other ETS factors through an ETS switching mechanism. These findings highlight the critical role that transient ETV2 expression plays in the regulation of hematopoietic and endothelial cell lineage specification and stability.

摘要

ETS 因子 ETV2(又名 ER71)对于血液和血管系统的生成至关重要,因为 ETV2 缺陷会导致血液和内皮细胞形成完全受阻,并致使小鼠胚胎致死。然而,ETV2 介导的基因调控网络以及控制造血和内皮细胞发育的信号传导机制却鲜为人知。在此,我们绘制了 ETV2 的全基因组结合位点图谱,开展了胚胎干细胞的体外分化研究,以及种系和条件性基因敲除小鼠研究,以揭示中胚层向血管生成命运定向分化所涉及的机制。我们发现 ETV2 与指定造血和内皮细胞谱系的增强子结合。我们发现发育胚胎中的血管生成祖细胞群体可被鉴定为 FLK1(高)PDGFRα(-)。值得注意的是,这些血管生成祖细胞对 ETV2 依赖的 FLK1 信号传导具有独特的敏感性。重要的是,ETV2 开启了其他 Ets 基因,从而建立了一个 ETS 层级体系。因此,由 ETV2 启动的造血和内皮细胞程序部分地通过 ETS 转换机制由其他 ETS 因子维持。这些发现凸显了短暂的 ETV2 表达在调节造血和内皮细胞谱系指定及稳定性方面所起的关键作用。

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