The histone H3K4 demethylase JARID1A directly interacts with haematopoietic transcription factor GATA1 in erythroid cells through its second PHD domain
The histone H3K4 demethylase JARID1A directly interacts with haematopoietic transcription factor GATA1 in erythroid cells through its second PHD domain
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DOI：
10.1098/rsos.191048
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发表时间：
2020-01
影响因子：
3.5
通讯作者：
D. Karia;Robert C. G. Gilbert;Antonio J. Biasutto;C. Porcher;E. Mancini
中科院分区：
文献类型：
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作者：
D. Karia;Robert C. G. Gilbert;Antonio J. Biasutto;C. Porcher;E. Mancini
染色质重塑和转录因子通过控制基因表达在谱系承诺和发育中发挥重要作用。选择的谱系特异性基因的激活和替代的谱系附属基因的抑制导致严格调控的细胞分化转录程序。然而，转录因子和染色质修饰酶之间复杂的功能和物理相互作用仍然难以捉摸。最近的证据表明，组蛋白去甲基酶与正常的造血分化以及恶性造血有关。在这里，我们报道了H3K4去甲基酶JARID1A与红细胞中造血特异性主转录蛋白SCL和GATA1之间的相互作用。具体地说，我们观察到GATA1与JARID1A的第二个PHD结构域之间有直接的物理接触。这种相互作用对正常和恶性造血有潜在的影响。
Chromatin remodelling and transcription factors play important roles in lineage commitment and development through control of gene expression. Activation of selected lineage-specific genes and repression of alternative lineage-affiliated genes result in tightly regulated cell differentiation transcriptional programmes. However, the complex functional and physical interplay between transcription factors and chromatin-modifying enzymes remains elusive. Recent evidence has implicated histone demethylases in normal haematopoietic differentiation as well as in malignant haematopoiesis. Here, we report an interaction between H3K4 demethylase JARID1A and the haematopoietic-specific master transcription proteins SCL and GATA1 in red blood cells. Specifically, we observe a direct physical contact between GATA1 and the second PHD domain of JARID1A. This interaction has potential implications for normal and malignant haematopoiesis.