Symmetry Breaking in the Life Cycle of the Budding Yeast
Symmetry Breaking in the Life Cycle of the Budding Yeast
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DOI：
10.1101/cshperspect.a003384
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发表时间：
2009-09-01
影响因子：
7.2
通讯作者：
Li, Rong
中科院分区：
文献类型：
--
作者：
Slaughter, Brian D.;Smith, Sarah E.;Li, Rong
芽殖酵母酿酒酵母一直是研究响应特定生理信号而建立细胞不对称性和生长极性的宝贵模型系统。大量实验观察表明，即使没有任何预先存在的外部不对称性，酵母细胞也能够通过两个耦合且部分冗余的内在机制打破对称性并建立极性。其中一种机制依赖于肌动蛋白细胞骨架和 Rho 家族 GTPase Cdc42 之间的相互作用，而另一种机制则依赖于 Cdc42 GTPase 信号网络。这些机制的组成部分似乎是能够放大小的随机不对称性的正反馈循环。空间线索，例如芽痕和信息素梯度，通过调节 Cdc42 GTPase 循环的调节来定向细胞极性，从而使不对称扩增的位点产生偏差。
The budding yeast Saccharomyces cerevisiae has been an invaluable model system for the study of the establishment of cellular asymmetry and growth polarity in response to specific physiological cues. A large body of experimental observations has shown that yeast cells are able to break symmetry and establish polarity through two coupled and partially redundant intrinsic mechanisms, even in the absence of any pre-existing external asymmetry. One of these mechanisms is dependent upon interplay between the actin cytoskeleton and the Rho family GTPase Cdc42, whereas the other relies on a Cdc42 GTPase signaling network. Integral to these mechanisms appear to be positive feedback loops capable of amplifying small and stochastic asymmetries. Spatial cues, such as bud scars and pheromone gradients, orient cell polarity by modulating the regulation of the Cdc42 GTPase cycle, thereby biasing the site of asymmetry amplification.