Runge Svenja, Bilgen Ecenaz, Magni Andrea, Bonollo Giorgio, Colombo Giorgio, Itzen Aymelt, Lamb Don C
Department of Biochemistry and Signal Transduction, University Medical Center Hamburg-Eppendorf, Hamburg 20246, Germany.
Department of Chemistry and Center for Nanoscience, Ludwig-Maximilians-Universität Munich, Munich 81377, Germany.
Proc Natl Acad Sci U S A. 2025 Aug 26;122(34):e2500079122. doi: 10.1073/pnas.2500079122. Epub 2025 Aug 21.
The human Fic enzyme FicD plays an important role in regulating the Hsp70 homolog BiP in the endoplasmic reticulum: FicD reversibly modulates BiP's activity through attaching an adenosine monophosphate to the substrate binding domain. This reduces BiP's chaperone activity by shifting it into a conformation with reduced substrate affinity. Crystal structures of FicD in the apo, adenosine triphosphate (ATP)-bound, and BiP-bound states suggested significant conformational variability in the tetratricopeptide repeat (TPR) motifs. However, nothing is known about the underlying dynamics. In this study, we investigate the conformational dynamics of FicD's TPR motifs using two-color, single-molecule Förster resonance energy transfer (smFRET) experiments. We demonstrate that the TPR motifs exhibit conformational dynamics between a TPR-out and a TPR-in conformation on timescales ranging from microseconds to milliseconds. In addition, we extend our investigation on multiple labeling positions within FicD, revealing how conformational dynamics vary depending on the location within the TPR motif. We quantify the motions with dynamic photon distribution analysis for the FRET constructs and generate an ensemble of structures for the different states consistent with the smFRET data using molecular dynamic simulations. We propose a conformational landscape model for FicD where the TPR-in/out states exist in equilibrium and the fraction of dynamic population is altered due to the presence of ATP and BiP. These results indicate that not only is FicD dynamic, but the dynamics are linked to the functionality and interactions of FicD with BiP.
人类Fic酶FicD在内质网中对热休克蛋白70同源物BiP的调节起着重要作用:FicD通过将单磷酸腺苷连接到底物结合域来可逆地调节BiP的活性。这通过将BiP转变为底物亲和力降低的构象来降低其伴侣活性。FicD在无配体、结合三磷酸腺苷(ATP)和结合BiP状态下的晶体结构表明,四肽重复(TPR)基序存在显著的构象变异性。然而,对于其潜在的动力学却一无所知。在本研究中,我们使用双色单分子Förster共振能量转移(smFRET)实验研究了FicD的TPR基序的构象动力学。我们证明,TPR基序在从微秒到毫秒的时间尺度上,在TPR-out和TPR-in构象之间表现出构象动力学。此外,我们扩展了对FicD内多个标记位置的研究,揭示了构象动力学如何根据TPR基序内的位置而变化。我们使用FRET构建体的动态光子分布分析对运动进行量化,并使用分子动力学模拟为与smFRET数据一致的不同状态生成一组结构。我们提出了一个FicD的构象景观模型,其中TPR-in/out状态处于平衡状态,并且由于ATP和BiP的存在,动态群体的比例会发生变化。这些结果表明,不仅FicD是动态的,而且动力学与FicD与BiP的功能和相互作用相关联。