Section on Membrane Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA.
Section on Membrane Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA.
J Biol Chem. 2021 Jan-Jun;296:100411. doi: 10.1016/j.jbc.2021.100411. Epub 2021 Feb 11.
Formations of myofibers, osteoclasts, syncytiotrophoblasts, and fertilized zygotes share a common step, cell-cell fusion. Recent years have brought about considerable progress in identifying some of the proteins involved in these and other cell-fusion processes. However, even for the best-characterized cell fusions, we still do not know the mechanisms that regulate the timing of cell-fusion events. Are they fully controlled by the expression of fusogenic proteins or do they also depend on some triggering signal that activates these proteins? The latter scenario would be analogous to the mechanisms that control the timing of exocytosis initiated by Ca influx and virus-cell fusion initiated by low pH- or receptor interaction. Diverse cell fusions are accompanied by the nonapoptotic exposure of phosphatidylserine at the surface of fusing cells. Here we review data on the dependence of membrane remodeling in cell fusion on phosphatidylserine and phosphatidylserine-recognizing proteins and discuss the hypothesis that cell surface phosphatidylserine serves as a conserved "fuse me" signal regulating the time and place of cell-fusion processes.
肌纤维、破骨细胞、合胞滋养层和受精卵的形成都有一个共同的步骤，即细胞-细胞融合。近年来，在鉴定这些和其他细胞融合过程中涉及的一些蛋白质方面取得了相当大的进展。然而，即使对于研究得最好的细胞融合，我们仍然不知道调节细胞融合事件时间的机制。它们是否完全受融合蛋白的表达控制，还是也依赖于激活这些蛋白的某种触发信号？后一种情况类似于由 Ca 流入引发的胞吐作用和由低 pH 或受体相互作用引发的病毒-细胞融合的时间控制机制。不同的细胞融合伴随着融合细胞表面磷脂酰丝氨酸的非凋亡暴露。在这里，我们回顾了关于细胞融合中膜重塑对磷脂酰丝氨酸和磷脂酰丝氨酸识别蛋白的依赖性的数据，并讨论了这样一种假设，即细胞表面磷脂酰丝氨酸作为一种保守的“融合我”信号，调节细胞融合过程的时间和地点。
