A cluster of neural crest cells (NCCs) may chemotax up a shallow external gradient to which a single cell is unresponsive. To explain this intriguing 'group advantage', we propose a chemo-mechanical model based on the signaling proteins Rac1 and RhoA. We represent each cell as a polygon with nodes connected by elastic membranes. Via reaction-diffusion on the membrane and exchange with their cytosolic pools, Rac1 and RhoA interact to produce cell polarization and repolarization subject to random noise. Mechanically, we represent cell motility via overdamped nodal motion subject to passive elastic membrane forces and active protrusive or contractile forces where Rac1 or RhoA dominates. The model reproduces the random walk of a single cell in a weak gradient and two modes of cell-cell interaction: contact inhibition of locomotion and co-attraction. The simultaneous action of contact inhibition and co-attraction suppresses random Rac1 bursts on the membrane and serves to preserve existing protrusions. This amounts to an emergent persistence of polarity that markedly enhances the ability of a cluster of NCCs to chemotax in a weak gradient against random noise, thereby giving rise to the group advantage.

中文翻译：

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基于Rho-GTPase的模型解释了神经rest细胞集体趋化性中的组优势。

神经c细胞（NCC）簇可能在一个浅的外部梯度上起化学趋化作用，单个细胞对此无反应。为了解释这种有趣的“群体优势”，我们提出了一种基于信号蛋白Rac1和RhoA的化学机械模型。我们将每个单元表示为具有通过弹性膜连接的节点的多边形。通过在膜上的反应扩散并与它们的胞质池交换，Rac1和RhoA相互作用，产生细胞极化和受到随机噪声影响的重新极化。从机械上讲，我们通过过度阻尼的节点运动来表示细胞运动，其中节点运动受到被动的弹性膜力和主动的突出或收缩力的作用，其中Rac1或RhoA占主导地位。该模型再现了弱梯度中单个细胞的随机游动以及两种细胞-细胞相互作用的模式：运动和共同吸引力的接触抑制。接触抑制和共吸引的同时作用抑制了膜上随机出现的Rac1突增，并保留了现有的突起。这相当于出现了极性的持久性，从而显着增强了NCC簇以弱梯度抵抗随机噪声进行化学趋化的能力，从而带来了群体优势。