Competition and collaboration between different actin assembly pathways allows for homeostatic control of the actin cytoskeleton.
Competition and collaboration between different actin assembly pathways allows for homeostatic control of the actin cytoskeleton.
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DOI：
10.1080/19490992.2015.1090670
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发表时间：
2014-01-01
期刊：
影响因子：
--
通讯作者：
Bear, James E
中科院分区：
文献类型：
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作者：
Rotty, Jeremy D;Bear, James E
对肌动蛋白相关蛋白的深入了解来自于对其活性和调节的仔细的生物化学和细胞生物学表征。然而，许多关于它们的细胞行为的研究只是孤立地考虑每一种。最近的努力表明，组装因子竞争聚合能力的肌动蛋白单体，这表明肌动蛋白是稳态调节。它似乎是一个主要的调节成分Arp 2/3激活成核促进因子和profilin肌动蛋白单体之间的竞争。结果是肌动蛋白向不同途径的差异递送，允许同时组装竞争性F-肌动蛋白结构和协作构建更高级的细胞结构。虽然有可能是额外的因素，调节肌动蛋白的稳态，特别是在一个细胞类型依赖的方式，我们提出的概念，肌动蛋白组装因子之间的竞争导致一个可调的系统，可以根据细胞外和细胞内的线索进行调整。
Tremendous insight into actin-associated proteins has come from careful biochemical and cell biological characterization of their activities and regulation. However, many studies of their cellular behavior have only considered each in isolation. Recent efforts reveal that assembly factors compete for polymerization-competent actin monomers, suggesting that actin is homeostatically regulated. It seems that a major regulatory component is competition between Arp2/3-activating nucleation promoting factors and profilin for actin monomers. The result is differential delivery of actin to different pathways, allowing for simultaneous assembly of competing F-actin structures and collaborative building of higher order cellular structures. Although there are likely to be additional factors that regulate actin homeostasis, especially in a cell type-dependent fashion, we advance the notion that competition between actin assembly factors results in a tunable system that can be adjusted according to extracellular and intracellular cues.