Many roads to symmetry breaking: molecular mechanisms and theoretical models of yeast cell polarity.
Many roads to symmetry breaking: molecular mechanisms and theoretical models of yeast cell polarity.
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DOI：
10.1091/mbc.e16-10-0739
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发表时间：
2017-02-01
影响因子：
3.3
通讯作者：
Leda M
中科院分区：
文献类型：
--
作者：
Goryachev AB;Leda M
数学建模有助于确定不同系统中细胞极性的共同原则。这些原理包括使细胞的空间均匀状态不稳定所需的正反馈回路。保守的小G蛋白Cdc 42是真核细胞极化的主要调节因子。在这里，我们讨论了Cdc 42极化在出芽和分裂酵母的研究的最新进展，并证明模型描述的破胶极化可以分为六个最小类的基础上的结构的正反馈回路激活和本地化Cdc 42。由于其通用的系统独立的性质，这些模型类也可能是相关的G-蛋白为基础的破坏系统的高等真核生物。我们回顾了实验证据支持和反对不同的理论上合理的模型，并得出结论，几个平行的和非相互排斥的机制可能参与酵母细胞极化。在解释最近的细胞重布线研究结果时，需要考虑到这种潜在的冗余。
Mathematical modeling has been instrumental in identifying common principles of cell polarity across diverse systems. These principles include positive feedback loops that are required to destabilize a spatially uniform state of the cell. The conserved small G-protein Cdc42 is a master regulator of eukaryotic cellular polarization. Here we discuss recent developments in studies of Cdc42 polarization in budding and fission yeasts and demonstrate that models describing symmetry-breaking polarization can be classified into six minimal classes based on the structure of positive feedback loops that activate and localize Cdc42. Owing to their generic system-independent nature, these model classes are also likely to be relevant for the G-protein–based symmetry-breaking systems of higher eukaryotes. We review experimental evidence pro et contra different theoretically plausible models and conclude that several parallel and non–mutually exclusive mechanisms are likely involved in cellular polarization of yeasts. This potential redundancy needs to be taken into consideration when interpreting the results of recent cell-rewiring studies.