Bhattacharjee Sayan, Sengupta Jayati
Division of Structural Biology and Bioinformatics, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Division of Structural Biology and Bioinformatics, CSIR-Indian Institute of Chemical Biology, Kolkata, India; Academy of Scientific and Innovative Research, Ghaziabad, India.
Biophys J. 2021 Oct 19;120(20):4512-4524. doi: 10.1016/j.bpj.2021.08.037. Epub 2021 Sep 1.
Molecular recognition is fundamental to transcription regulation. As a transcription factor, the tumor suppressor p53 has to recognize either specific DNA sequences or repressor protein partners. However, the molecular mechanism underlying the p53 conformational switch from the DNA-bound to repressor-bound states is not fully characterized. The highly charged nature of these interacting molecules prompted us to explore the nonbonded energy contributions behind molecular recognition of either a DNA or the repressor protein iASPP by p53 DNA binding domain (p53DBD), using molecular dynamics simulation followed by rigorous analyses of energy terms. Our results illuminate the allosteric pathway by which iASPP binding to p53 diminishes binding affinity between p53 and DNA. Even though the p53DBD uses a common framework of residues for recognizing both DNA and iASPP, a comparison of the electrostatics in the two p53DBD complexes revealed significant differences in residue-wise contributions to the electrostatic energy. We found that an electrostatic allosteric communication path exists in the presence of both substrates. It consists of evolutionarily conserved residues, from residue K120 of the binding loop L1 to a distal residue R213 of p53DBD. K120 is near the DNA in the p53DBD-DNA complex, whereas iASPP binding moves it away from its DNA binding position in the p53DBD-iASPP complex. The "energy hubs" (the residues show a higher degree of connectivity with other residues in the electrostatic networks) determined from the electrostatic network analysis established that this conformational change in K120 completely rewires the electrostatic network from K120 to R213, thereby impeding DNA binding. Furthermore, we found shifting populations of hydrogen bonds and salt bridges reduce pairwise electrostatic energies within p53DBD in its DNA-bound state.
分子识别是转录调控的基础。作为一种转录因子,肿瘤抑制因子p53必须识别特定的DNA序列或阻遏蛋白伴侣。然而,p53从DNA结合状态转变为阻遏蛋白结合状态的分子机制尚未完全明确。这些相互作用分子的高电荷性质促使我们利用分子动力学模拟并对能量项进行严格分析,来探索p53 DNA结合结构域(p53DBD)对DNA或阻遏蛋白iASPP进行分子识别背后的非键合能量贡献。我们的结果阐明了iASPP与p53结合降低p53与DNA之间结合亲和力的变构途径。尽管p53DBD使用共同的残基框架来识别DNA和iASPP,但对两种p53DBD复合物中静电作用的比较揭示了残基对静电能贡献在逐个残基上的显著差异。我们发现在两种底物都存在的情况下存在一条静电变构通信路径。它由进化上保守的残基组成,从结合环L1的残基K120到p53DBD的远端残基R213。在p53DBD-DNA复合物中,K120靠近DNA,而iASPP的结合使其在p53DBD-iASPP复合物中远离其DNA结合位置。通过静电网络分析确定的“能量枢纽”(这些残基在静电网络中与其他残基显示出更高程度的连接性)表明,K120的这种构象变化完全重新连接了从K120到R213的静电网络,从而阻碍了DNA结合。此外,我们发现氢键和盐桥的群体转移降低了处于DNA结合状态的p53DBD内的成对静电能。