Endocytosis switch controlled by transmembrane osmotic pressure and phospholipid number asymmetry
Endocytosis switch controlled by transmembrane osmotic pressure and phospholipid number asymmetry
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DOI：
10.1016/s0006-3495(00)76842-1
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发表时间：
2000-06-01
影响因子：
3.4
通讯作者：
Farge, E
中科院分区：
文献类型：
--
作者：
Rauch, C;Farge, E
降低外源介质渗透压，增加跨膜磷脂数目不对称性，观察活K562细胞内吞作用的动态变化。当外压降低0.54倍时，观察到内吞作用突然受到抑制。在此条件下，在磷脂数目不对称性增加后，内吞作用突然恢复。磷脂的不对称性是通过外源磷脂酰丝氨酸的加入而产生的，外源磷脂酰丝氨酸通过内源翻转酶的活性转移到膜的内层。因此，内吞作用的恢复与磷脂数量不对称可以作为内吞作用的萌芽力量的观点是一致的。此外，我们使用假设跨膜表面张力不对称的存在作为萌发驱动力的一般模型，定量地预测了内吞作用的抑制和恢复都是一级相变。在该模型中，张力不对称被认为是由磷脂泵送活动弹性地产生的。我们最后提出，细胞因子-受体复合体内化后，细胞可能触发遗传转录反应，这可能受胞浆或外压变化的控制。
The dynamics of endocytosis in living K562 cells was investigated after the osmotic pressure of the external medium was decreased and the transmembrane phospholipid number asymmetry was increased. When the external pressure was decreased by a factor of 0.54, a sudden inhibition of endocytosis was observed. Under these conditions, the endocytosis suddenly recovered after the phospholipid number asymmetry was increased. The phospholipid asymmetry was generated by the addition of exogenous phosphatidylserine, which is translocated by the endogenous flippase activity to the inner layer of the membrane. The recovery of endocytosis is thus consistent with the view that the phospholipid number asymmetry can act as a budding force for endocytosis. Moreover, we quantitatively predict both the inhibition and recovery of endocytosis as first-order phase transitions, using a general model that assumes the existence of a transmembrane surface tension asymmetry as the budding driving force. In this model, the tension asymmetry is considered to be elastically generated by the activity of phospholipid pumping. We finally propose that cells may trigger genetic transcription responses after the internalization of cytokine-receptor complexes, which could be controlled by variations in the cytosolic or external pressure.