Jain Neha, Narang Dominic, Bhasne Karishma, Dalal Vijit, Arya Shruti, Bhattacharya Mily, Mukhopadhyay Samrat
Department of Biological Sciences, Indian Institute of Science Education and Research (IISER), Mohali, Knowledge City, S.A.S. Nagar, Mohali, Punjab, India.
Centre for Protein Science, Design, and Engineering, Indian Institute of Science Education and Research (IISER), Mohali, Knowledge City, S.A.S. Nagar, Mohali, Punjab, India; Department of Biological Sciences, Indian Institute of Science Education and Research (IISER), Mohali, Knowledge City, S.A.S. Nagar, Mohali, Punjab, India.
Biophys J. 2016 Aug 23;111(4):768-774. doi: 10.1016/j.bpj.2016.07.023.
The fundamental backbone dynamics of unfolded proteins arising due to intrinsic ϕ-ψ dihedral angle fluctuations dictate the course of protein folding, binding, assembly, and function. These internal fluctuations are also critical for protein misfolding associated with a range of human diseases. However, direct observation and unambiguous assignment of this inherent dynamics in chemically denatured proteins is extremely challenging due to various experimental limitations. To directly map the backbone torsional mobility in the ϕ-ψ dihedral angle space, we used a model intrinsically disordered protein, namely, α-synuclein, that adopts an expanded state under native conditions. We took advantage of nonoccurrence of tryptophan in α-synuclein and created a number of single-tryptophan variants encompassing the entire polypeptide chain. We then utilized highly sensitive picosecond time-resolved fluorescence depolarization measurements that allowed us to discern the site-specific torsional relaxation at a low protein concentration under physiological conditions. For all the locations, the depolarization kinetics exhibited two well-separated rotational-correlation-time components. The shorter, subnanosecond component arises due to the local mobility of the indole side chain, whereas the longer rotational-correlation-time component (1.37 ± 0.15 ns), independent of global tumbling, represents a characteristic timescale for short-range conformational exchange in the ϕ-ψ dihedral space. This correlation time represents an intrinsic timescale for torsional relaxation and is independent of position, which is expected for an extended polypeptide chain having little or no propensity to form persistent structures. We were also able to capture this intrinsic timescale at the N-terminal unstructured domain of the prion protein. Our estimated timescale of the segmental mobility is similar to that of unfolded proteins studied by nuclear magnetic resonance in conjunction with molecular dynamics simulations. Our results have broader implications for a diverse range of functionally and pathologically important intrinsically disordered proteins and disordered regions.
由内在的ϕ-ψ二面角波动引起的未折叠蛋白质的基本骨架动力学决定了蛋白质折叠、结合、组装和功能的进程。这些内部波动对于与一系列人类疾病相关的蛋白质错误折叠也至关重要。然而,由于各种实验限制,在化学变性蛋白质中直接观察和明确确定这种固有动力学极具挑战性。为了直接绘制ϕ-ψ二面角空间中的骨架扭转流动性,我们使用了一种模型内在无序蛋白质,即α-突触核蛋白,它在天然条件下处于扩展状态。我们利用α-突触核蛋白中不存在色氨酸这一特点,创建了许多涵盖整个多肽链的单色氨酸变体。然后,我们利用高灵敏度的皮秒时间分辨荧光去极化测量,使我们能够在生理条件下的低蛋白质浓度下辨别位点特异性扭转弛豫。对于所有位置,去极化动力学表现出两个明显分开的旋转相关时间分量。较短的亚纳秒分量是由于吲哚侧链的局部流动性引起的,而较长的旋转相关时间分量(1.37±0.15纳秒),与整体翻滚无关,代表了ϕ-ψ二面角空间中短程构象交换的特征时间尺度。这个相关时间代表了扭转弛豫的固有时间尺度,并且与位置无关,这对于几乎没有或没有形成持久结构倾向的延伸多肽链来说是预期的。我们还能够在朊病毒蛋白的N端非结构化结构域捕获这个固有时间尺度。我们估计的片段流动性时间尺度与通过核磁共振结合分子动力学模拟研究的未折叠蛋白质的时间尺度相似。我们的结果对各种功能和病理上重要的内在无序蛋白质和无序区域具有更广泛的意义。