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Symmetry breaking in a bulk-surface reaction-diffusion model for signalling networks

机译:信号网络的体表反应扩散模型的对称性破缺

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摘要

Signalling molecules play an important role for many cellular functions. We investigate here a general system of two membrane reaction-diffusion equations coupled to a diffusion equation inside the cell by a Robin-type boundary condition and a flux term in the membrane equations. A specific model of this form was recently proposed by the authors for the GTPase cycle in cells. We investigate here a putative role of diffusive instabilities in cell polarization. By a linearized stability analysis, we identify two different mechanisms. The first resembles a classical Turing instability for the membrane subsystem and requires (unrealistically) large differences in the lateral diffusion of activator and substrate. On the other hand, the second possibility is induced by the difference in cytosolic and lateral diffusion and appears much more realistic. We complement our theoretical analysis by numerical simulations that confirm the new stability mechanism and allow us to investigate the evolution beyond the regime where the linearization applies.
机译:信号分子对许多细胞功能起着重要作用。我们在这里研究由两个膜反应扩散方程耦合到细胞内部的扩散方程的一般系统,该扩散方程通过Robin型边界条件和膜方程中的通量项。作者最近针对细胞中的GTPase循环提出了这种形式的特定模型。我们在这里调查扩散不稳定性在细胞极化中的推定作用。通过线性化稳定性分析,我们确定了两种不同的机制。第一种类似于膜子系统的经典图灵不稳定性,并且要求(不切实际地)活化剂和底物的横向扩散存在较大差异。另一方面,第二种可能性是由胞浆和侧向扩散的差异引起的,并且显得更为现实。我们通过数值模拟对理论分析进行补充,这些数值模拟确认了新的稳定性机制,并允许我们研究线性化应用范围之外的演变。

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