Endosomal membrane tension regulates ESCRT-III-dependent intra-lumenal vesicle formation.

Endosomal membrane tension regulates ESCRT-III-dependent intra-lumenal vesicle formation.
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DOI:
10.1038/s41556-020-0546-4
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发表时间:
2020-08
影响因子:
21.3
通讯作者:
Roux A
Roux A
中科院分区:
生物学1区
文献类型:
--
作者:
Mercier V;Larios J;Molinard G;Goujon A;Matile S;Gruenberg J;Roux A

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质膜张力强烈影响细胞表面过程,例如迁移、内吞作用和信号传导。然而,尚不清楚细胞器的膜张力是否调节其功能,特别是细胞内的交通。 ESCRT-III 复合物是主要的膜重塑复合物,可驱动内体膜上的腔内囊泡 (ILV) 形成。在这里,我们利用荧光膜张力探针来表明,当膜张力降低时,ESCRT-III 亚基被招募到内体膜上。我们发现张力依赖性募集与体外 ESCRT-III 聚合和膜变形相关,并且与体内 ESCRT-III 修饰的内体中 ILV 形成增加相关。最后,我们发现在生理条件下,当 EGF 触发 ILV 形成时,内体膜张力降低。这些结果表明膜张力是 ILV 形成和内体运输的主要调节因子,使我们得出结论膜张力可以控制细胞器功能。
Plasma membrane tension strongly affects cell surface processes, such as migration, endocytosis and signalling. However, it is not known whether membrane tension of organelles regulates their functions, notably intracellular traffic. The ESCRT-III complex is the major membrane remodelling complex that drives Intra-Lumenal Vesicle (ILV) formation on endosomal membranes. Here, we made use of a fluorescent membrane tension probe to show that ESCRT-III subunits are recruited onto endosomal membranes when membrane tension is reduced. We find that tension-dependent recruitment is associated with ESCRT-III polymerization and membrane deformation in vitro, and correlates with increased ILV formation in ESCRT-III decorated endosomes in vivo. Finally, we find that endosomal membrane tension decreases when ILV formation is triggered by EGF under physiological conditions. These results indicate that membrane tension is a major regulator of ILV formation and of endosome trafficking, leading us to conclude that membrane tension can control organelle functions.
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