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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The mediator complex functions as a coactivator for GATA-1 in erythropoiesis via subunit Medl/TRAP220
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The mediator complex functions as a coactivator for GATA-1 in erythropoiesis via subunit Medl/TRAP220

机译：介体复合物通过亚基Medl / TRAP220在红细胞生成中充当GATA-1的共激活因子

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摘要

The Mediator complex forms the bridge between transcriptional activators and RNA polymerase II. Mediator subunit Med1/TRAP220 is a key component of Mediator originally found to associate with nuclear hormone receptors. Med1 deficiency causes lethality at embryonic day 11.5 because of defects in heart and placenta development. Here we show that Med1-deficient 10.5 days postcoitum embryos are anemic but have normal numbers of hematopoietic progenitor cells. Med1-deficient progenitor cells have a defect in forming erythroid burst-forming units (BFU-E) and colony-forming units (CFU-E), but not in forming myeloid colonies. At the molecular level, we demonstrate that Med1 interacts physically with the erythroid master regulator GATA-1. In transcription assays, Med1 deficiency leads to a defect in GATA-1-mediated transactivation. In chromatin immunoprecipitation experiments, we find Mediator components at GATA-1-occupied enhancer sites. Thus, we conclude that Mediator subunit Med1 acts as a pivotal coactivator for GATA-1 in erythroid development.
机译：介体复合物形成转录激活剂和RNA聚合酶II之间的桥梁。介体亚基Med1 / TRAP220是介体的关键成分，最初被发现与核激素受体相关。 Med1缺乏症在胚胎第11.5天会导致致死性，因为心脏和胎盘发育存在缺陷。在这里，我们显示，Med1缺乏的10.5天后，coitumum胚胎贫血，但具有正常数量的造血祖细胞。 Med1缺陷的祖细胞在形成类红细胞爆发形成单位（BFU-E）和菌落形成单位（CFU-E）方面存在缺陷，但在形成骨髓集落方面则没有缺陷。在分子水平上，我们证明Med1与类红细胞主调节剂GATA-1发生物理相互作用。在转录测定中，Med1缺陷导致GATA-1介导的反式激活存在缺陷。在染色质免疫沉淀实验中，我们在GATA-1占据的增强子位点发现介体成分。因此，我们得出结论，介体亚基Med1在红系发育中充当GATA-1的关键共激活因子。

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