Department of Mechanical and Aerospace Engineering, Sapienza Università di Roma, Rome, Italy.
Sci Rep. 2024 Jan 2;14(1):23. doi: 10.1038/s41598-023-50922-7.
Viral infections, fertilization, neurotransmission, and many other fundamental biological processes rely on membrane fusion. Straightforward calculations based on the celebrated Canham-Helfrich elastic model predict a large topological energy barrier that prevents the fusion process from being thermally activated. While such high energy is in accordance with the physical barrier function of lipid membranes, it is difficult to reconcile with the biological mechanisms involved in fusion processes. In this work, we use a Ginzburg-Landau type of free energy that recovers the Canham-Helfrich model in the limit of small width-to-vesicle-extension ratio, with the additional ability to handle topological transitions. We show that a local modification of the Gaussian modulus in the merging region both dramatically lowers the elastic energy barrier and substantially changes the minimal energy pathway for fusion, in accordance with experimental evidence. Therefore, we discuss biological examples in which such a modification might play a crucial role.
病毒感染、受精、神经递质传递以及许多其他基本的生物学过程都依赖于膜融合。基于著名的 Canham-Helfrich 弹性模型的简单计算预测,融合过程会受到一个很大的拓扑能量障碍的阻碍,使其无法被热激活。虽然这种高能量与脂质膜的物理屏障功能一致,但与融合过程中涉及的生物学机制很难协调。在这项工作中,我们使用了一种类似于 Ginzburg-Landau 的自由能,在小的宽度-囊泡延伸比极限下恢复了 Canham-Helfrich 模型,并且具有处理拓扑转变的额外能力。我们表明,在融合区域局部修改高斯模量既可以显著降低弹性能量障碍,又可以大大改变融合的最小能量途径,这与实验证据一致。因此,我们讨论了在生物学中,这种修改可能会起到关键作用的例子。