Gan Wan Jun, Motegi Fumio
Temasek Life-Sciences Laboratory, Singapore, Singapore.
Department of Biological Sciences, National University of Singapore, Singapore, Singapore.
Front Cell Dev Biol. 2021 Jan 18;8:619869. doi: 10.3389/fcell.2020.619869. eCollection 2020.
Cell polarity is the asymmetric organization of cellular components along defined axes. A key requirement for polarization is the ability of the cell to break symmetry and achieve a spatially biased organization. Despite different triggering cues in various systems, symmetry breaking (SB) usually relies on mechanochemical modulation of the actin cytoskeleton, which allows for advected movement and reorganization of cellular components. Here, the mechanisms underlying SB in zygote, one of the most popular models to study cell polarity, are reviewed. A zygote initiates SB through the centrosome, which modulates mechanics of the cell cortex to establish advective flow of cortical proteins including the actin cytoskeleton and partitioning defective (PAR) proteins. The chemical signaling underlying centrosomal control of the Aurora A kinase-mediated cascade to convert the organization of the contractile actomyosin network from an apolar to polar state is also discussed.
细胞极性是细胞成分沿特定轴的不对称组织。极化的一个关键要求是细胞打破对称性并实现空间偏向组织的能力。尽管在各种系统中有不同的触发线索，但对称性打破（SB）通常依赖于肌动蛋白细胞骨架的机械化学调节，这允许细胞成分的平流运动和重组。在这里，我们综述了合子中对称性打破的潜在机制，合子是研究细胞极性最常用的模型之一。合子通过中心体启动对称性打破，中心体调节细胞皮层的力学，以建立包括肌动蛋白细胞骨架和PAR（partitioning defective）蛋白在内的皮层蛋白的平流。还讨论了中心体控制极光A激酶介导的级联反应以将收缩性肌动球蛋白网络的组织从非极性转变为极性状态的化学信号传导。
