Collective action by Inverse-BAR (I-BAR) domains drive micron-scale membrane remodeling. The macroscopic curvature sensing and generation behavior of I-BAR domains is well characterized, and computational models have suggested various mechanisms on simplified membrane systems, but there remain missing connections between the complex environment of the cell and the models proposed thus far. Here, we show a connection between the role of protein curvature and lipid clustering in the relaxation of large membrane deformations. When we include PIP2-like lipids that preferentially interact with the charged ends of an I-BAR domain, we find clustering of PIP2-like lipids that induces a directional membrane-mediated interaction between membrane-bound I-BAR domains. Lipid clusters mediate I-BAR domain interactions and cause I-BAR domain aggregates that would not arise through membrane fluctuation-based or curvature-based interactions. Inside of membrane protrusions, lipid cluster-mediated interaction draws long side-by-side aggregates together resulting in more cylindrical protrusions as opposed to bulbous, irregularly shaped protrusions.

中文翻译：

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脂质成分介导的力可以稳定 I-BAR 蛋白的管状组装

Inverse-BAR (I-BAR) 域的集体作用驱动微米级膜重塑。I-BAR 域的宏观曲率传感和生成行为得到了很好的表征，计算模型已经提出了简化膜系统的各种机制，但细胞的复杂环境与迄今为止提出的模型之间仍然存在缺失的联系。在这里，我们展示了蛋白质曲率和脂质聚集在大膜变形松弛中的作用之间的联系。当我们包括优先与 I-BAR 结构域的带电末端相互作用的 PIP2 样脂质时，我们发现 PIP2 样脂质的聚集会诱导膜结合 I-BAR 结构域之间的定向膜介导的相互作用。脂质簇介导 I-BAR 结构域相互作用并导致 I-BAR 结构域聚集体，这些聚集体不会通过基于膜波动或基于曲率的相互作用产生。在膜突起内部，脂质簇介导的相互作用将长的并排聚集体拉在一起，导致更多的圆柱形突起，而不是球状、不规则形状的突起。