Rowland Michael A, Harrison Brian, Deeds Eric J
Center for Computational Biology, University of Kansas, Lawrence, Kansas.
Center for Computational Biology, University of Kansas, Lawrence, Kansas; Department of Molecular Biosciences, University of Kansas, Lawrence, Kansas; Santa Fe Institute, Santa Fe, New Mexico.
Biophys J. 2015 Feb 17;108(4):986-996. doi: 10.1016/j.bpj.2014.12.011.
Phosphatases play an important role in cellular signaling networks by regulating the phosphorylation state of proteins. Phosphatases are classically considered to be promiscuous, acting on tens to hundreds of different substrates. We recently demonstrated that a shared phosphatase can couple the responses of two proteins to incoming signals, even if those two substrates are from otherwise isolated areas of the network. This finding raises a potential paradox: if phosphatases are indeed highly promiscuous, how do cells insulate themselves against unwanted crosstalk? Here, we use mathematical models to explore three possible insulation mechanisms. One approach involves evolving phosphatase KM values that are large enough to prevent saturation by the phosphatase's substrates. Although this is an effective method for generating isolation, the phosphatase becomes a highly inefficient enzyme, which prevents the system from achieving switch-like responses and can result in slow response kinetics. We also explore the idea that substrate degradation can serve as an effective phosphatase. Assuming that degradation is unsaturatable, this mechanism could insulate substrates from crosstalk, but it would also preclude ultrasensitive responses and would require very high substrate turnover to achieve rapid dephosphorylation kinetics. Finally, we show that adaptor subunits, such as those found on phosphatases like PP2A, can provide effective insulation against phosphatase crosstalk, but only if their binding to substrates is uncoupled from their binding to the catalytic core. Analysis of the interaction network of PP2A's adaptor domains reveals that although its adaptors may isolate subsets of targets from one another, there is still a strong potential for phosphatase crosstalk within those subsets. Understanding how phosphatase crosstalk and the insulation mechanisms described here impact the function and evolution of signaling networks represents a major challenge for experimental and computational systems biology.
磷酸酶通过调节蛋白质的磷酸化状态在细胞信号网络中发挥重要作用。传统上认为磷酸酶具有多特异性,可作用于数十到数百种不同的底物。我们最近证明,一种共享的磷酸酶可以将两种蛋白质的反应与传入信号耦合起来,即使这两种底物来自网络中其他相互隔离的区域。这一发现引发了一个潜在的悖论:如果磷酸酶确实具有高度的多特异性,那么细胞如何使自身免受不必要的串扰呢?在这里,我们使用数学模型来探索三种可能的隔离机制。一种方法是使磷酸酶的米氏常数(KM值)足够大,以防止其底物饱和。虽然这是产生隔离的有效方法,但磷酸酶会变成一种效率极低的酶,这会阻止系统实现类似开关的反应,并可能导致缓慢的反应动力学。我们还探讨了底物降解可作为一种有效磷酸酶的观点。假设降解是不饱和的,这种机制可以使底物免受串扰,但它也会排除超敏感反应,并且需要非常高的底物周转率才能实现快速的去磷酸化动力学。最后,我们表明,衔接子亚基,如在PP2A等磷酸酶上发现的那些亚基,可以提供有效的隔离以防止磷酸酶串扰,但前提是它们与底物的结合与其与催化核心的结合解耦。对PP2A衔接子结构域相互作用网络的分析表明,虽然其衔接子可能会使目标子集相互隔离,但在这些子集中仍存在很强的磷酸酶串扰可能性。理解磷酸酶串扰以及此处描述的隔离机制如何影响信号网络的功能和进化,是实验和计算系统生物学面临的一项重大挑战。