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具有膨压的细胞中内吞作用的膜力学

Membrane Mechanics of Endocytosis in Cells with Turgor.

作者信息

Dmitrieff Serge, Nédélec François

机构信息

Cell Biology and Biophysics Unit, European Molecular Biology Laboratory, Heidelberg, Germany.

出版信息

PLoS Comput Biol. 2015 Oct 30;11(10):e1004538. doi: 10.1371/journal.pcbi.1004538. eCollection 2015 Oct.

DOI:10.1371/journal.pcbi.1004538
PMID:26517669
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4627814/
Abstract

Endocytosis is an essential process by which cells internalize a piece of plasma membrane and material from the outside. In cells with turgor, pressure opposes membrane deformations, and increases the amount of force that has to be generated by the endocytic machinery. To determine this force, and calculate the shape of the membrane, we used physical theory to model an elastic surface under pressure. Accurate fits of experimental profiles are obtained assuming that the coated membrane is highly rigid and preferentially curved at the endocytic site. The forces required from the actin machinery peaks at the onset of deformation, indicating that once invagination has been initiated, endocytosis is unlikely to stall before completion. Coat proteins do not lower the initiation force but may affect the process by the curvature they induce. In the presence of isotropic curvature inducers, pulling the tip of the invagination can trigger the formation of a neck at the base of the invagination. Hence direct neck constriction by actin may not be required, while its pulling role is essential. Finally, the theory shows that anisotropic curvature effectors stabilize membrane invaginations, and the loss of crescent-shaped BAR domain proteins such as Rvs167 could therefore trigger membrane scission.

摘要

内吞作用是细胞将一段质膜和外部物质内化的重要过程。在具有膨压的细胞中,压力会阻碍膜的变形,并增加内吞机制必须产生的力量。为了确定这种力量并计算膜的形状,我们使用物理理论对受压的弹性表面进行建模。假设被包被的膜具有高刚性且在内吞位点优先弯曲,就能获得与实验轮廓的精确拟合。肌动蛋白机制所需的力量在变形开始时达到峰值,这表明一旦内陷开始,内吞作用在完成之前不太可能停滞。包被蛋白不会降低起始力量,但可能通过它们诱导的曲率影响这一过程。在存在各向同性曲率诱导剂的情况下,拉动内陷的尖端可触发在内陷基部形成颈部。因此,肌动蛋白直接的颈部收缩可能不是必需的,但其拉动作用至关重要。最后,该理论表明各向异性曲率效应器可稳定膜内陷,因此诸如Rvs167等新月形BAR结构域蛋白的缺失可能会触发膜分裂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/b2ff12715f5e/pcbi.1004538.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/deeb6962ea54/pcbi.1004538.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/228f803599b5/pcbi.1004538.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/5f45e1035d25/pcbi.1004538.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/24ab566fd8fb/pcbi.1004538.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/b7219216beee/pcbi.1004538.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/b2ff12715f5e/pcbi.1004538.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/deeb6962ea54/pcbi.1004538.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/228f803599b5/pcbi.1004538.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/5f45e1035d25/pcbi.1004538.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/24ab566fd8fb/pcbi.1004538.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/b7219216beee/pcbi.1004538.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c49/4627814/b2ff12715f5e/pcbi.1004538.g006.jpg

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