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FBXO11-mediated proteolysis of BAHD1 relieves PRC2-dependent transcriptional repression in erythropoiesis.

FBXO11-mediated BAHD1的蛋白水解缓解红细胞生成中的PRC2-dependent转录抑制。

  • 影响因子:7.27
  • DOI:10.1182/blood.2020007809
  • 作者列表:"Xu P","Scott DC","Xu B","Yao Y","Feng R","Cheng L","Mayberry K","Wang YD","Bi W","Palmer LE","King MT","Wang H","Li Y","Fan Y","Alpi AF","Li C","Peng J","Papizan J","Pruett-Miller SM","Spallek R","Bassermann F","Cheng Y","Schulman BA","Weiss MJ
  • 发表时间:2021-01-14
Abstract

:The histone mark H3K27me3 and its reader/writer polycomb repressive complex 2 (PRC2) mediate widespread transcriptional repression in stem and progenitor cells. Mechanisms that regulate this activity are critical for hematopoietic development but are poorly understood. Here we show that the E3 ubiquitin ligase F-box only protein 11 (FBXO11) relieves PRC2-mediated repression during erythroid maturation by targeting its newly identified substrate bromo adjacent homology domain-containing 1 (BAHD1), an H3K27me3 reader that recruits transcriptional corepressors. Erythroblasts lacking FBXO11 are developmentally delayed, with reduced expression of maturation-associated genes, most of which harbor bivalent histone marks at their promoters. In FBXO11-/- erythroblasts, these gene promoters bind BAHD1 and fail to recruit the erythroid transcription factor GATA1. The BAHD1 complex interacts physically with PRC2, and depletion of either component restores FBXO11-deficient erythroid gene expression. Our studies identify BAHD1 as a novel effector of PRC2-mediated repression and reveal how a single E3 ubiquitin ligase eliminates PRC2 repression at many developmentally poised bivalent genes during erythropoiesis.

摘要

: 组蛋白标记H3K27me3及其读写器polycomb抑制复合物2 (PRC2) 介导干细胞和祖细胞中广泛的转录抑制。调节这种活性的机制对造血发育至关重要,但了解甚少。在这里,我们展示了E3泛素连接酶F-box only蛋白11 (FBXO11) 通过靶向其新鉴定的底物溴相邻同源结构域1 (BAHD1),一种招募转录辅助抑制因子的H3K27me3阅读器,缓解了红系成熟过程中的PRC2-mediated抑制。缺乏FBXO11的成红细胞是发育延迟的,成熟相关基因的表达减少,其中大部分在其启动子处具有二价组蛋白标记。在FBXO11-/-成红细胞体中,这些基因启动子结合BAHD1而不能募集红系转录因子gata1。BAHD1复合物与PRC2物理相互作用,任一组分的耗尽恢复FBXO11-deficient红系基因表达。我们的研究确定BAHD1是PRC2-mediated抑制的新效应物,并揭示了单个E3泛素连接酶如何在红细胞生成过程中消除许多发育平衡二价基因的PRC2抑制。

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DOI:10.1007/s11033-021-06299-9
作者列表:["Louvrier A","Terranova L","Meyer C","Meyer F","Euvrard E","Kroemer M","Rolin G"]

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