Proteins become asymmetrically distributed in the one-cell Caenorhabditis elegans embryo thanks to reaction–diffusion mechanisms that are often entangled in complex feedback loops. Cortical polarity drives the enrichment of the RNA-binding proteins MEX-5 and MEX-6 in the anterior cytoplasm through concentration gradients. MEX-5 and MEX-6 promote the patterning of other cytoplasmic factors, including that of the anteriorly enriched mitotic polo-like kinase PLK-1, but also contribute to proper cortical polarity. The gradient of MEX-5 forms through a differential-diffusion mechanism. How MEX-6 establishes a gradient and how MEX-5 and MEX-6 regulate cortical polarity is not known. Here, we reveal that the two MEX proteins develop concentration asymmetries via similar mechanisms, but despite their strong sequence homology, they differ in terms of how their concentration gradients are regulated. We find that PLK-1 promotes the enrichment of MEX-5 and MEX-6 at the anterior through different circuits: PLK-1 influences the MEX-5 gradient indirectly by regulating cortical polarity while it modulates the formation of the gradient of MEX-6 through its physical interaction with the protein. We thus propose a model in which PLK-1 mediates protein circuitries between MEX-5, MEX-6, and cortical proteins to faithfully establish and maintain polarity.

中文翻译：

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MEX-5、MEX-6 和 PLK-1 之间的内部反馈电路在秀丽隐杆线虫胚胎中保持忠实的模式


由于反应扩散机制经常纠缠在复杂的反馈回路中，蛋白质在单细胞秀丽隐杆线虫胚胎中变得不对称分布。皮质极性通过浓度梯度驱动前细胞质中 RNA 结合蛋白 MEX-5 和 MEX-6 的富集。MEX-5 和 MEX-6 促进其他细胞质因子的模式化，包括前部富集的有丝分裂 polo 样激酶 PLK-1 的模式化，但也有助于适当的皮质极性。MEX-5 的梯度通过差分扩散机制形成。MEX-6 如何建立梯度以及 MEX-5 和 MEX-6 如何调节皮质极性尚不清楚。在这里，我们揭示了两种 MEX 蛋白通过相似的机制产生浓度不对称，但尽管它们具有很强的序列同源性，但它们在浓度梯度的调节方式方面有所不同。我们发现 PLK-1 通过不同的回路促进 MEX-5 和 MEX-6 在前部的富集：PLK-1 通过调节皮质极性间接影响 MEX-5 梯度，同时通过与蛋白质的物理相互作用调节 MEX-6 梯度的形成。因此，我们提出了一个模型，其中 PLK-1 介导 MEX-5、MEX-6 和皮质蛋白之间的蛋白质回路，以忠实地建立和维持极性。