Membrane Shape Instability Induced by Protein Crowding
Membrane Shape Instability Induced by Protein Crowding
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DOI：
10.1016/j.bpj.2016.09.039
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发表时间：
2016-11-01
影响因子：
3.4
通讯作者：
Baumgart, Tobias
中科院分区：
文献类型：
--
作者：
Chen, Zhiming;Atefi, Ehsan;Baumgart, Tobias
外周蛋白可以通过几种不同的机制使膜弯曲，包括支架化、楔入、寡聚化和拥挤。尤其是拥挤效应最近受到了相当大的关注，部分原因是它是一种依数性机制，这意味着它原则上可以被任何外周蛋白质探索。在这里，我们试图澄清在何种程度上利用这种机制的内吞辅助蛋白。我们定量研究膜曲率的产生通过GUV形状稳定性测定。我们发现，诱导膜弯曲所需的拥挤量与膜张力相关。重要的是，我们还发现，在相同的膜张力，拥挤机制需要更高的蛋白覆盖率，以诱导曲率变化相比，所观察到的内嗜蛋白BAR结构域，在这里作为一个例子的内吞辅助蛋白。我们的研究结果是重要的膜靶向生物传感器的设计，以及生物膜成形的机制的理解。
Peripheral proteins can bend membranes through several different mechanisms, including scaffolding, wedging, oligomerization, and crowding. The crowding effect in particular has received considerable attention recently, in part because it is a colligative mechanism-implying that it could, in principle, be explored by any peripheral protein. Here we sought to clarify to what extent this mechanism is exploited by endocytic accessory proteins. We quantitatively investigate membrane curvature generation by means of a GUV shape stability assay. We found that the amount of crowding required to induce membrane curvature is correlated with membrane tension. Importantly, we also revealed that at the same membrane tension, the crowding mechanism requires far higher protein coverage to induce curvature changes compared to those observed for the endophilin BAR domain, serving here as an example of an endocytic accessory protein. Our results are important for the design of membrane-targeted biosensors as well as the understanding of mechanisms of biological membrane shaping.