在单细胞C中建立PAR蛋白极性的模型。秀丽隐杆线虫胚胎
Modelling the Establishment of PAR Protein Polarity in the One-Cell C. elegans Embryo
摘要：
在单细胞阶段，C. elegans胚胎沿前后轴极化。PAR蛋白在细胞骨架重排驱动的动态过程中形成互补的前部和后部结构域。最初，PAR蛋白均匀分布在整个胚胎中。在受精的提示下，皮层肌动球蛋白向前极收缩。PAR-3/PAR-6/PKC-3（前部PAR蛋白）仅限于前部皮质。PAR-1和PAR-2（后部PAR蛋白）在后部皮质区域富集。我们提出了一个数学模型的极性建立过程中，我们采取了一种新的方法，结合反应扩散动力学的PAR蛋白耦合到一个简单的模型肌动球蛋白收缩。我们表明，PAR蛋白之间已知的相互作用足以解释野生型和突变胚胎中观察到的皮质PAR动态的许多方面。然而，细胞质PAR蛋白的极性，这是至关重要的子细胞产生不同的分子成分，不能在这样一个框架内得到适当的解释。因此，我们考虑额外的机制，可以重现适当的细胞质极性。特别是我们预测，在细胞质中的细胞骨架的不对称性，除了皮质肌动球蛋白的不对称性，是一个重要的决定因素PAR蛋白定位。
英文摘要：
At the one-cell stage, the C. elegans embryo becomes polarized along the anterior-posterior axis. The PAR proteins form complementary anterior and posterior domains in a dynamic process driven by cytoskeletal rearrangement. Initially, the PAR proteins are uniformly distributed throughout the embryo. Following a cue from fertilization, cortical actomyosin contracts towards the anterior pole. PAR-3/PAR-6/PKC-3 (the anterior PAR proteins) become restricted to the anterior cortex. PAR-1 and PAR-2 (the posterior PAR proteins) become enriched in the posterior cortical region. We present a mathematical model of this polarity establishment process, in which we take a novel approach to combine reaction-diffusion dynamics of the PAR proteins coupled to a simple model of actomyosin contraction. We show that known interactions between the PAR proteins are sufficient to explain many aspects of the observed cortical PAR dynamics in both wild-type and mutant embryos. However, cytoplasmic PAR protein polarity, which is vital for generating daughter cells with distinct molecular components, cannot be properly explained within such a framework. We therefore consider additional mechanisms that can reproduce the proper cytoplasmic polarity. In particular we predict that cytoskeletal asymmetry in the cytoplasm, in addition to the cortical actomyosin asymmetry, is a critical determinant of PAR protein localization.
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