Molecular Physiology, and Molecular Medicine Research Group, School of Medicine, Western Sydney University, Campbelltown Campus, Penrith, NSW 2751, Australia.
Faculty of Graduate Studies and the Departments of Health Sciences and Biological Sciences, Brock University,St. Catharines, ON L2S 3A1, Canada.
Int J Biochem Cell Biol. 2017 Apr;85:1-5. doi: 10.1016/j.biocel.2017.01.011. Epub 2017 Jan 25.
Membrane fusion is a fundamental molecular mechanism by which two apposed membrane bilayers coalesce in rapid, transient steps that enable the successive merging of the outer and inner leaflets allowing lipid intermixing and subsequent mixing of the two previously separate compartments. The actual membrane merger mechanism - fusion, by definition - is conceptualized to be protein- or lipid-centric. According to the widely vetted stalk-pore hypothesis, membrane fusion proceeds via high curvature lipid intermediates. By cleaving membrane phospholipids at the sn-2 position, Phospholipase A generates metabolites that exert spontaneous curvature stress (both negative and positive) on the membrane, thus influencing local membrane bending by altering the packing and conformation of lipids and proteins, respectively. Such changes could potentially modulate priming and attachment/docking steps that precede fusion, as well as the membrane merger steps per se.
膜融合是一种基本的分子机制,通过该机制,两个相邻的膜双层在快速、瞬间的步骤中融合,使外叶和内叶连续融合,允许脂质混合,随后将两个先前分离的隔室混合。根据广泛验证的柄孔假说,膜融合是通过高曲率脂质中间体进行的。通过在 sn-2 位置切割膜磷脂,磷脂酶 A 产生代谢物,对膜施加自发曲率应力(正和负),从而通过改变脂质和蛋白质的包装和构象来分别影响局部膜弯曲。这些变化可能会调节融合前的引发和附着/对接步骤,以及膜融合本身的步骤。