Department of Chemistry , State University of New York at Stony Brook , Stony Brook , New York 11794 , United States.
Department of Biomedical Sciences, College of Medicine , Florida State University , Tallahassee , Florida 32306 , United States.
J Chem Theory Comput. 2020 Feb 11;16(2):1319-1332. doi: 10.1021/acs.jctc.9b01146. Epub 2020 Jan 30.
Proteins in vivo endure highly various interactions from the luxuriant surrounding macromolecular cosolutes. Confinement and macromolecular crowding are the two major effects that should be considered while comparing the results of protein dynamics from in vitro to in vivo. However, efforts have been largely focused on single domain protein folding up to now, and the quantifications of the in vivo effects in terms of confinements and crowders on modulating the structure and dynamics as well as the physical understanding of the underlying mechanisms on multidomain protein folding are still challenging. Here we developed a topology-based model to investigate folding of a multidomain Y-family DNA polymerase (DPO4) within spherical confined space and in the presence of repulsive and attractive crowders. We uncovered that the entropic component of the thermodynamic driving force led by confinements and repulsive crowders increases the stability of folded states relative to the folding intermediates and unfolded states, while the enthalpic component of the thermodynamic driving force led by attractive crowders gives rise to the opposite effects with less stability. We found that the shapes of DPO4 conformations influenced by the confinements and the crowders are quite different even when only the entropic component of the thermodynamic driving force is considered. We uncovered that under all in vivo conditions, the folding cooperativity of DPO4 decreases compared to that in bulk. We showed that the loss of folding cooperativity can promote the sequential domain-wise folding, which was widely found in cotranslational multidomain protein folding, and effectively prohibit the backtracking led by topological frustrations during multidomain protein folding processes.
蛋白质在体内会经历丰富多样的相互作用,这些相互作用来自于周围丰富的大分子共溶剂。在比较蛋白质动力学的体外和体内结果时,应该考虑到限制和大分子拥挤这两个主要影响因素。然而,到目前为止,研究主要集中在单域蛋白质折叠上,对于限制和拥挤对调节结构和动力学的体内影响的量化,以及对多域蛋白质折叠的物理理解,仍然具有挑战性。在这里,我们开发了一种基于拓扑的模型,用于研究多域 Y 家族 DNA 聚合酶(DPO4)在球形受限空间内和存在排斥性和吸引性共溶剂时的折叠情况。我们发现,限制和排斥性共溶剂导致的热力学驱动力的熵分量增加了折叠态相对于折叠中间体和未折叠态的稳定性,而吸引性共溶剂导致的热力学驱动力的焓分量则产生了相反的效果,稳定性降低。我们发现,即使只考虑热力学驱动力的熵分量,限制和共溶剂对 DPO4 构象的影响形状也有很大的不同。我们发现,与在本体相相比,在所有体内条件下,DPO4 的折叠协同性降低。我们表明,折叠协同性的丧失可以促进顺序的域间折叠,这在共翻译的多域蛋白质折叠中广泛存在,并有效地防止拓扑障碍在多域蛋白质折叠过程中导致的回溯。