Monine Michael I, Haugh Jason M
Department of Chemical and Biomolecular Engineering, North Carolina State University, Raleigh, North Carolina 27695, USA.
Biophys J. 2008 Sep;95(5):2172-82. doi: 10.1529/biophysj.108.128892. Epub 2008 May 23.
The plasma membrane provides a physical platform for the orchestration of molecular interactions and biochemical conversions involved in the early stages of receptor-mediated signal transduction in living cells. In that context, we introduce here the concept of spatial coupling, wherein simultaneous recruitment of different enzymes to the same receptor scaffold facilitates crosstalk between different signaling pathways through the local release and capture of activated signaling molecules. To study the spatiotemporal dynamics of this mechanism, we have developed a Brownian dynamics modeling approach and applied it to the receptor-mediated activation of Ras and the cooperative recruitment of phosphoinositide 3-kinase (PI3K) by activated receptors and Ras. Various analyses of the model simulations show that cooperative assembly of multimolecular complexes nucleated by activated receptors is facilitated by the local release and capture of membrane-anchored signaling molecules (such as active Ras) from/by receptor-bound signaling proteins. In the case of Ras/PI3K crosstalk, the model predicts that PI3K is more likely to be recruited by activated receptors bound or recently visited by the enzyme that activates Ras. By this mechanism, receptor-bound PI3K is stabilized through short-range, diffusion-controlled capture of active Ras and Ras/PI3K complexes released from the receptor complex. We contend that this mechanism is a means by which signaling pathways are propagated and spatially coordinated for efficient crosstalk between them.
质膜为活细胞中受体介导的信号转导早期阶段所涉及的分子相互作用和生化转化的协调提供了一个物理平台。在此背景下,我们在此引入空间偶联的概念,即同时将不同的酶招募到同一受体支架上,通过局部释放和捕获活化的信号分子促进不同信号通路之间的串扰。为了研究这一机制的时空动态,我们开发了一种布朗动力学建模方法,并将其应用于受体介导的Ras激活以及活化受体和Ras对磷酸肌醇3激酶(PI3K)的协同招募。对模型模拟的各种分析表明,由活化受体成核的多分子复合物的协同组装通过从受体结合的信号蛋白中局部释放和捕获膜锚定信号分子(如活性Ras)而得到促进。在Ras/PI3K串扰的情况下,该模型预测PI3K更有可能被激活Ras的酶结合或最近访问过的活化受体招募。通过这种机制,受体结合的PI3K通过对从受体复合物释放的活性Ras和Ras/PI3K复合物进行短程、扩散控制的捕获而得以稳定。我们认为这种机制是信号通路得以传播并在空间上协调以实现它们之间有效串扰的一种方式。