Profilin and formin constitute a pacemaker system for robust actin filament growth
Profilin and formin constitute a pacemaker system for robust actin filament growth
复制标题
DOI：
10.7554/elife.50963
复制
发表时间：
2019-10-24
期刊：
影响因子：
7.7
通讯作者：
Bieling, Peter
中科院分区：
文献类型：
--
作者：
Funk, Johanna;Merino, Felipe;Bieling, Peter
肌动蛋白细胞骨架驱动许多基本的生物学过程，从细胞形态发生到运动。功能性肌动蛋白网络的组装需要控制肌动蛋白丝生长的速度。在细胞中发现的高水平和可变水平的可溶性肌动蛋白亚基如何实现这一点尚不清楚。在这里，我们重组装配哺乳动物，非肌肉肌动蛋白丝从生理浓度的profilin-actin。我们发现，在这些条件下，长丝生长是有限的profilin从长丝端解离和伸长的速度变得不敏感的可溶性亚基的浓度。甚至在饱和的profilin-actin浓度下，profilin-actin聚合酶也可以直接促进Profilin的释放。我们证明，哺乳动物细胞确实在限制肌动蛋白丝的生长所施加的profilin和formins。我们的研究结果揭示了profilin和formins之间的协同作用如何产生强大的细丝生长速率，对可溶性亚基浓度的变化具有弹性。
The actin cytoskeleton drives many essential biological processes, from cell morphogenesis to motility. Assembly of functional actin networks requires control over the speed at which actin filaments grow. How this can be achieved at the high and variable levels of soluble actin subunits found in cells is unclear. Here we reconstitute assembly of mammalian, non-muscle actin filaments from physiological concentrations of profilin-actin. We discover that under these conditions, filament growth is limited by profilin dissociating from the filament end and the speed of elongation becomes insensitive to the concentration of soluble subunits. Profilin release can be directly promoted by formin actin polymerases even at saturating profilin-actin concentrations. We demonstrate that mammalian cells indeed operate at the limit to actin filament growth imposed by profilin and formins. Our results reveal how synergy between profilin and formins generates robust filament growth rates that are resilient to changes in the soluble subunit concentration.