Barethiya Shrishti, Schultz Samantha, Zhang Yumeng, Chen Jianhan
Department of Chemistry, University of Massachusetts, Amherst, Massachusetts 01003, United States.
Molecular and Cellular Biology Program, University of Massachusetts, Amherst, Massachusetts 01003, United States.
Biochemistry. 2025 Apr 1;64(7):1636-1645. doi: 10.1021/acs.biochem.4c00668. Epub 2025 Mar 18.
Intrinsically disordered proteins (IDPs) are key components of cellular signaling and regulatory networks. They frequently remain dynamic even in complexes and thus rely on potentially subtle shifts in the disordered conformational ensemble for function. Understanding the molecular basis of these fascinating mechanisms of IDP function and regulation requires a detailed characterization of dynamic ensembles in various biologically relevant states. Here, we study the phosphorylation dependence of the dynamic interaction between the N-terminal transactivation domain (NTAD) and DNA-binding domain (DBD) of tumor suppressor p53, which plays a key role in the autoinhibition and regulation of p53 activation or termination during various stages of stress response. By extending the hybrid-resolution (HyRes) coarse-grained (CG) protein force field to model phosphorylated side chains, we show that HyRes simulations accurately recapitulate the effects of phosphorylation on the p53 NTAD/DBD interactions. The simulated ensembles show that phosphorylation of Thr55 as well as Ser46 enhances dynamic NTAD/DBD interactions and further induces conformational shifts that promote trans interactions between two p53 dimers to drive dissociation from DNA. These CG simulations thus provide a strong molecular basis in support of previous experimental studies suggesting the central role of dynamic interactions of disordered domains and phosphorylation in the function of p53. The success of this study also suggests that HyRes provides an efficient and viable tool for studying dynamic interactions and post-translational modifications in IDP function and regulation.
内在无序蛋白质(IDP)是细胞信号传导和调控网络的关键组成部分。即使在复合物中,它们也常常保持动态,因此其功能依赖于无序构象集合中潜在的细微变化。要理解IDP功能和调控这些迷人机制的分子基础,需要详细表征各种生物学相关状态下的动态集合。在这里,我们研究了肿瘤抑制因子p53的N端反式激活结构域(NTAD)与DNA结合结构域(DBD)之间动态相互作用的磷酸化依赖性,p53在应激反应的各个阶段对自身抑制以及p53激活或终止的调控中起着关键作用。通过扩展混合分辨率(HyRes)粗粒度(CG)蛋白质力场以模拟磷酸化侧链,我们表明HyRes模拟能够准确概括磷酸化对p53 NTAD/DBD相互作用的影响。模拟集合表明,Thr55以及Ser46的磷酸化增强了NTAD/DBD的动态相互作用,并进一步诱导构象变化,促进两个p53二聚体之间的反式相互作用,从而驱动与DNA的解离。因此,这些CG模拟为支持先前的实验研究提供了强有力的分子基础,这些研究表明无序结构域的动态相互作用和磷酸化在p53功能中起着核心作用。这项研究的成功还表明,HyRes为研究IDP功能和调控中的动态相互作用及翻译后修饰提供了一种高效且可行的工具。