发表机构
Bhabha Atomic Research Centre; Homi Bhabha National Institute; Oak Ridge National Laboratory; Shiv Nadar Institution of Eminence（巴巴原子研究中心; 霍米·巴巴国家研究所; 橡树岭国家实验室; 希夫·纳达尔卓越机构）
机构由 AI 辅助整理，请以论文原文为准。AI 中文总结
本研究通过多种中子散射技术发现，抗菌肽aurein对膜力学性质的影响取决于膜组成：在DMPC中引起渐进软化，在含PG的膜中先软化后硬化，并揭示分子扩散与集体刚度在多尺度上的解耦。
AI 中文摘要
膜组成在决定抗菌肽（AMP）如何与脂质膜相互作用并改变其物理性质方面起着核心作用。在此，我们利用中子自旋回波（NSE）光谱、中子膜衍射（NMD）和压力（P）-面积（A）等温线，并结合先前报道的准弹性中子散射（QENS）测量，研究了脂质膜对aurein肽的组成依赖性力学和结构响应。在两性离子DMPC膜中，aurein诱导渐进式软化，表现为弯曲刚度和面积压缩模量均随浓度增加而降低。NMD揭示出轻微的膜变薄，但在氘化烃区域内没有显著的肽相关贡献，表明渐进式力学软化并未伴随肽向疏水核心的更深渗透。相比之下，含有阴离子磷脂酰甘油（PG）的DMPC/DMPG膜表现出非单调响应，先出现软化，随后在较高肽浓度下出现显著硬化。补充的P-A等温线测量独立地再现了这些对比鲜明的力学响应，显示DMPC渐进软化而DMPC/DMPG硬化。最重要的是，NSE和QENS结果的结合揭示了显著的多尺度解耦：aurein抑制分子尺度的脂质侧向扩散，同时降低介观尺度的集体膜刚度，证明在相同肽作用下，分子脂质动力学和集体膜力学可以沿相反方向演化。总之，这些结果表明膜组成决定了膜对aurein的集体力学响应，而分子脂质动力学可以在更短的长度和时间尺度上独立响应。
英文摘要
Membrane composition plays a central role in determining how antimicrobial peptides (AMPs) interact with and alter the physical properties of lipid membranes. Here, we investigate the composition-dependent mechanical and structural response of lipid membranes to the AMP aurein using neutron spin-echo (NSE) spectroscopy, neutron membrane diffraction (NMD), and pressure (P)-area (A) isotherms, complemented by previously reported quasielastic neutron scattering (QENS) measurements. In a zwitterionic DMPC membrane, aurein induces progressive softening, manifested by a concentration-dependent decrease in both the bending rigidity and area compressibility modulus. NMD reveals a slight bilayer thinning but no prominent peptide-associated contribution within the deuterated hydrocarbon region, indicating that the progressive mechanical softening is not accompanied by increasingly deep peptide penetration into the hydrophobic core. In contrast, anionic phosphatidylglycerol (PG)-containing DMPC/DMPG membranes exhibit a non-monotonic response, with initial softening followed by pronounced stiffening at higher peptide concentrations. Complementary P-A isotherm measurements independently reproduce these contrasting mechanical responses, showing progressive softening of DMPC but stiffening of DMPC/DMPG. Most importantly, the combined NSE and QENS results reveal a striking multiscale decoupling: aurein suppresses molecular-scale lipid lateral diffusion while simultaneously reducing collective membrane stiffness at the mesoscopic scale, demonstrating that molecular lipid dynamics and collective membrane mechanics can evolve in opposite directions under the same peptide perturbation.Together, these results show that membrane composition governs the collective mechanical response to aurein, while molecular lipid dynamics can respond independently at shorter length and time scales.
