Kasahara Kota, Shiina Masaaki, Fukuda Ikuo, Ogata Kazuhiro, Nakamura Haruki
College of Life Sciences, Ritsumeikan University, Kusatsu, Shiga, Japan.
Graduate School of Medicine, Yokohama City University, Kanazawa-ku, Yokohama, Kanagawa, Japan.
PLoS One. 2017 Feb 23;12(2):e0172654. doi: 10.1371/journal.pone.0172654. eCollection 2017.
Ets1 is an essential transcription factor (TF) for several important physiological processes, including cell proliferation and differentiation. Its recognition of the enhancer region of the TCRα gene is enhanced by the cooperative binding of the Runx1-CBFβ heterodimer, with the cancelation of phosphorylation-dependent autoinhibition. The detailed mechanism of this interesting cooperativity between Ets1 and the Runx1-CBFβ heterodimer is still largely unclear. Here, we investigated the molecular mechanisms of this cooperativity, by using molecular dynamics simulations. Consequently, we detected high flexibility of the loop region between the HI2 and H1 helices of Ets1. Upon Runx1-CBFβ heterodimer binding, this loop transiently adopts various sub-stable conformations in its interactions with the DNA. In addition, a network analysis suggested an allosteric pathway in the molecular assembly and identified some key residues that coincide with previous experimental studies. Our simulations suggest that the cooperative binding of Ets1 and the Runx1-CBFβ heterodimer alters the DNA conformation and induces sub-stable conformations of the HI2-H1 loop of Ets1. This phenomenon increases the flexibility of the regulatory module, including the HI2 helix, and destabilizes the inhibitory form of this module. Thus, we hypothesize that this effect facilitates Ets1-DNA binding and prevents the phosphorylation-dependent DNA binding autoinhibition.
Ets1是几种重要生理过程(包括细胞增殖和分化)所必需的转录因子(TF)。Runx1-CBFβ异二聚体的协同结合增强了它对TCRα基因增强子区域的识别,同时消除了磷酸化依赖性的自身抑制作用。Ets1与Runx1-CBFβ异二聚体之间这种有趣协同作用的详细机制在很大程度上仍不清楚。在这里,我们通过分子动力学模拟研究了这种协同作用的分子机制。结果,我们检测到Ets1的HI2和H1螺旋之间的环区域具有高灵活性。在Runx1-CBFβ异二聚体结合后,该环在与DNA相互作用时会短暂地采取各种亚稳定构象。此外,网络分析表明在分子组装中存在一条变构途径,并确定了一些与先前实验研究一致的关键残基。我们的模拟表明,Ets1与Runx1-CBFβ异二聚体的协同结合改变了DNA构象,并诱导了Ets1的HI2-H1环的亚稳定构象。这种现象增加了包括HI2螺旋在内的调节模块的灵活性,并使该模块的抑制形式不稳定。因此,我们假设这种效应促进了Ets1与DNA的结合,并防止了磷酸化依赖性的DNA结合自身抑制作用。