Dai J, Ting-Beall H P, Sheetz M P
Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
J Gen Physiol. 1997 Jul;110(1):1-10. doi: 10.1085/jgp.110.1.1.
Stimulated secretion in endocrine cells and neuronal synapses causes a rise in endocytosis rates to recover the added membrane. The endocytic process involves the mechanical deformation of the membrane to produce an invagination. Studies of osmotic swelling effects on endocytosis indicate that the increased surface tension is tightly correlated to a significant decrease of endocytosis. When rat basophilic leukemia (RBL) cells are stimulated to secrete, there is a dramatic drop in the membrane tension and only small changes in membrane bending stiffness. Neither the shape change that normally accompanies secretion nor the binding of ligand without secretion causes a drop in tension. Further, tension decreases within 6 s, preceding shape change and measurable changes in endocytosis. After secretion stops, tension recovers. On the basis of these results we suggest that the physical parameter of membrane tension is a major regulator of endocytic rate in RBL cells. Low tensions would stimulate endocytosis and high tensions would stall the endocytic machinery.
内分泌细胞和神经元突触中的刺激分泌会导致内吞率上升,以回收增加的膜。内吞过程涉及膜的机械变形以产生内陷。关于渗透肿胀对内吞作用影响的研究表明,表面张力的增加与内吞作用的显著降低密切相关。当大鼠嗜碱性白血病(RBL)细胞受到刺激而分泌时,膜张力会急剧下降,而膜弯曲刚度仅有微小变化。无论是通常伴随分泌的形状变化,还是无分泌情况下配体的结合,都不会导致张力下降。此外,张力在6秒内下降,早于形状变化和内吞作用中可测量的变化。分泌停止后,张力恢复。基于这些结果,我们认为膜张力的物理参数是RBL细胞内吞率的主要调节因子。低张力会刺激内吞作用,而高张力会使内吞机制停滞。