Naqvi Mohsin M, Zacharopoulou Maria, Saha Satyaki, Banerjee Anupam, Yilmaz Zeynep S, Sunderlikova Vanda, Johnson Chris M, Kumita Janet R, Yang Shang-Hua, Gordon Reuven, Ohlmeyer Michael, Tans Sander, Gur Mert, Bahar Ivet, Itzhaki Laura S
Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge CB2 1PD, UK.
Laufer Center for Physical and Quantitative Biology, Stony Brook University, NY 11794, USA, and Department of Biochemistry and Cell Biology, Renaissance School of Medicine, Stony Brook University, NY 11794, USA.
bioRxiv. 2025 Jul 29:2025.07.24.666388. doi: 10.1101/2025.07.24.666388.
Protein phosphatase 2A (PP2A), an important therapeutic target, comprises a scaffold subunit PR65 composed of 15 HEAT (Huntingtin/elongation/A-subunit/TOR1) repeats, a catalytic subunit, and one of many different regulatory subunits that enable binding to specific substrates. Recently, small molecule activators of PP2A (SMAPs) were identified, although their mechanisms of action have not been fully defined. Here we explore the interaction of PR65 with two SMAPs, ATUX-8385 and the non-functional DBK-776, using single-molecule optical tweezers, ensemble methods, and computational analysis. In the absence of SMAP, PR65 shows multiple unfolding and refolding transitions, and the force-extension profiles are very heterogeneous with evidence of misfolding. Similar heterogeneity has been observed for chemical-induced unfolding of tandem-repeat proteins like PR65, a consequence of the internal symmetry of the repeat architecture. In the presence of ATUX-8385, higher unfolding and refolding forces are observed globally, and there is less misfolding, suggesting that ATUX-8385 acts like a pharmacological chaperone. In contrast, DBK-766-binding induces higher unfolding forces for only a few repeats of PR65, suggestive of a more localised effect; moreover, subsequent stretch-relax cycles show that PR65 is irreversibly locked in the unfolded state. Docking and molecular dynamics simulations provide additional insights how SMAP binding modulates PR65 structure and function.
蛋白磷酸酶2A(PP2A)是一个重要的治疗靶点,它由一个由15个HEAT(亨廷顿蛋白/延伸因子/A亚基/TOR1)重复序列组成的支架亚基PR65、一个催化亚基以及众多不同调节亚基中的一个组成,这些调节亚基能够使其与特定底物结合。最近,PP2A的小分子激活剂(SMAPs)已被鉴定出来,尽管其作用机制尚未完全明确。在这里,我们使用单分子光镊、整体方法和计算分析,探索PR65与两种SMAPs(ATUX-8385和无功能的DBK-776)之间的相互作用。在没有SMAP的情况下,PR65显示出多个解折叠和重新折叠转变,并且力-伸长曲线非常不均匀,有错误折叠的迹象。对于像PR65这样的串联重复蛋白的化学诱导解折叠也观察到了类似的不均匀性,这是重复结构内部对称性的结果。在存在ATUX-8385的情况下,整体上观察到更高的解折叠和重新折叠力,并且错误折叠较少,这表明ATUX-8385的作用类似于一种药理伴侣。相比之下,DBK-766的结合仅对PR65的少数几个重复序列诱导出更高的解折叠力,提示其作用更具局部性;此外,随后的拉伸-松弛循环表明PR65不可逆地锁定在解折叠状态。对接和分子动力学模拟为SMAP结合如何调节PR65的结构和功能提供了更多见解。