Tchounwou Christine, Jobanputra Anjali J, Lasher Dylan, Fletcher Bretton J, Jacinto Jorge, Bhaduri Arjun, Best Rebecca L, Fisher William S, Ewert Kai K, Li Youli, Feinstein Stuart C, Safinya Cyrus R
Materials Department, University of California, Santa Barbara, California 93106, USA.
Molecular, Cellular, and Developmental Biology Department, University of California, Santa Barbara, California 93106, USA.
bioRxiv. 2024 Jul 17:2024.07.15.603342. doi: 10.1101/2024.07.15.603342.
Tau, an intrinsically disordered neuronal protein and polyampholyte with an overall positive charge, is a microtubule (MT) associated protein, which binds to anionic domains of MTs and suppresses their dynamic instability. Aberrant tau-MT interactions are implicated in Alzheimer's and other neurodegenerative diseases. Here, we studied the interactions between full length human protein tau and other negatively charged binding substrates, as revealed by differential-interference-contrast (DIC) and fluorescence microscopy. As a binding substrate, we chose anionic liposomes (ALs) containing either 1,2-dioleoyl-sn-glycero-3-phosphatidylserine (DOPS, -1e) or 1,2-dioleoyl-sn-glycero-3-phosphatidylglycerol (DOPG, -1e) mixed with zwitterionic 1,2dioleoyl-sn-glycero-3-phosphatidylcholine (DOPC) to mimic anionic plasma membranes of axons where tau resides. At low salt concentrations (0 to 10 mM KCl or NaCl) with minimal charge screening, reaction mixtures of tau and ALs resulted in the formation of distinct states of AL-tau complexes coexisting with liquid-liquid phase separated tau self-coacervates arising from the polyampholytic nature of tau containing cationic and anionic domains. AL-tau complexes exhibited distinct types of morphologies. This included, large ≈20-30 micron tau-decorated giant vesicles with additional smaller liposomes with bound tau attached to the giant vesicles, and tau-mediated finite-size assemblies of small liposomes. As the ionic strength of the solution was increased to near and above physiological salt concentrations for 1:1 electrolytes (≈150 mM), AL-tau complexes remained stable while tau self-coacervate droplets were found to dissolve indicative of breaking of (anionic/cationic) electrostatic bonds between tau chains due to increased charge screening. The findings are consistent with the hypothesis that distinct cationic domains of tau may interact with anionic lipid domains of the lumen facing monolayer of the axon plasma membrane suggesting the possibility of transient yet robust interactions at physiologically relevant ionic strengths.
tau蛋白是一种内在无序的神经元蛋白和具有整体正电荷的聚两性电解质,是一种微管(MT)相关蛋白,它与MT的阴离子结构域结合并抑制其动态不稳定性。异常的tau-MT相互作用与阿尔茨海默病和其他神经退行性疾病有关。在这里,我们通过微分干涉对比(DIC)和荧光显微镜研究了全长人tau蛋白与其他带负电荷的结合底物之间的相互作用。作为结合底物,我们选择了含有1,2-二油酰基-sn-甘油-3-磷脂酰丝氨酸(DOPS,-1e)或1,2-二油酰基-sn-甘油-3-磷脂酰甘油(DOPG,-1e)并与两性离子1,2-二油酰基-sn-甘油-3-磷脂酰胆碱(DOPC)混合的阴离子脂质体(ALs),以模拟tau蛋白所在轴突的阴离子质膜。在低盐浓度(0至10 mM KCl或NaCl)且电荷屏蔽最小的情况下,tau蛋白和ALs的反应混合物导致形成不同状态的AL-tau复合物,与由于含有阳离子和阴离子结构域的tau蛋白的聚两性电解质性质而产生的液-液相分离的tau蛋白自凝聚物共存。AL-tau复合物表现出不同类型的形态。这包括大约20-30微米的大的tau蛋白修饰的巨型囊泡,以及附着在巨型囊泡上的带有结合tau蛋白的额外较小脂质体,还有tau蛋白介导的小脂质体的有限尺寸组装体。随着溶液的离子强度增加到接近并高于1:1电解质的生理盐浓度(≈150 mM),AL-tau复合物保持稳定,而tau蛋白自凝聚液滴被发现溶解,这表明由于电荷屏蔽增加,tau蛋白链之间的(阴离子/阳离子)静电键断裂。这些发现与以下假设一致,即tau蛋白不同的阳离子结构域可能与轴突质膜内腔面向单层的阴离子脂质结构域相互作用,这表明在生理相关离子强度下可能存在短暂但强大的相互作用。