Department of Cell Biology, Harvard Medical School and Program in Cellular and Molecular Medicine at Boston Children's Hospital, Boston, Massachusetts 02115, USA.
Nat Cell Biol. 2012 Sep;14(9):906-8. doi: 10.1038/ncb2570.
It is widely assumed that peripheral membrane proteins induce intracellular membrane curvature by the asymmetric insertion of a protein segment into the lipid bilayer, or by imposing shape by adhesion of a curved protein domain to the membrane surface. Two papers now provide convincing evidence challenging these views. The first shows that specific assembly of a clathrin protein scaffold, coupled to the membrane, seems to be the most prevalent mechanism for bending a lipid bilayer in a cell. The second reports that membrane crowding, driven by protein-protein interactions, can also drive membrane bending, even in the absence of any protein insertion into the bilayer.
人们普遍认为，外周膜蛋白通过将蛋白质片段不对称地插入脂质双层，或者通过将弯曲的蛋白质域附着到膜表面来施加形状，从而诱导细胞内膜曲率。现在有两篇论文提供了令人信服的证据，挑战了这些观点。第一篇论文表明，网格蛋白蛋白支架的特定组装与膜结合，似乎是使脂质双层在细胞中弯曲的最常见机制。第二篇论文报道说，由蛋白质-蛋白质相互作用驱动的膜拥挤也可以驱动膜弯曲，即使没有任何蛋白质插入双层。
