Singh Shashi Prakash, Insall Robert H
CRUK Beatson Institute, Glasgow, UK.
Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.
Commun Integr Biol. 2020 Dec 28;14(1):1-4. doi: 10.1080/19420889.2020.1855854.
The Scar/WAVE complex catalyzes the protrusion of pseudopods and lamellipods, and is therefore a principal regulator of cell migration. However, it is unclear how its activity is regulated, beyond a dependence on Rac. Phosphorylation of the proline-rich region, by kinases such as Erk2, has been suggested as an upstream activator. We have recently reported that phosphorylation is not required for complex activation. Rather, it occurs after Scar/WAVE has been activated, and acts as a modulator. Neither chemoattractant signaling nor Erk2 affects the amount of phosphorylation, though in Dictyostelium it is promoted by cell-substrate adhesion. We now report that cell-substrate adhesion also promotes Scar/WAVE2 phosphorylation in mammalian cells, suggesting that the process is evolutionarily conserved.
Scar/WAVE复合体催化伪足和片状伪足的突出，因此是细胞迁移的主要调节因子。然而，除了对Rac的依赖性外，其活性如何调节尚不清楚。诸如Erk2等激酶对富含脯氨酸区域的磷酸化被认为是一种上游激活剂。我们最近报道，磷酸化对于复合体的激活并非必需。相反，它发生在Scar/WAVE被激活之后，并起调节剂的作用。趋化因子信号传导和Erk2均不影响磷酸化的量，不过在盘基网柄菌中，细胞-底物黏附可促进磷酸化。我们现在报道，细胞-底物黏附在哺乳动物细胞中也能促进Scar/WAVE2的磷酸化，这表明该过程在进化上是保守的。
