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Molecular Interactions of the Min Protein System Reproduce Spatiotemporal Patterning in Growing and Dividing Escherichia coli Cells

机译:最小蛋白系统的分子相互作用重现时空格局在成长和分裂的大肠杆菌细胞中。

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摘要

Oscillations of the Min protein system are involved in the correct midcell placement of the divisome during Escherichia coli cell division. Based on molecular interactions of the Min system, we formulated a mathematical model that reproduces Min patterning during cell growth and division. Specifically, the increase in the residence time of MinD attached to the membrane as its own concentration increases, is accounted for by dimerisation of membrane-bound MinD and its interaction with MinE. Simulation of this system generates unparalleled correlation between the waveshape of experimental and theoretical MinD distributions, suggesting that the dominant interactions of the physical system have been successfully incorporated into the model. For cells where MinD is fully-labelled with GFP, the model reproduces the stationary localization of MinD-GFP for short cells, followed by oscillations from pole to pole in larger cells, and the transition to the symmetric distribution during cell filamentation. Cells containing a secondary, GFP-labelled MinD display a contrasting pattern. The model is able to account for these differences, including temporary midcell localization just prior to division, by increasing the rate constant controlling MinD ATPase and heterotetramer dissociation. For both experimental conditions, the model can explain how cell division results in an equal distribution of MinD and MinE in the two daughter cells, and accounts for the temperature dependence of the period of Min oscillations. Thus, we show that while other interactions may be present, they are not needed to reproduce the main characteristics of the Min system in vivo.
机译:在大肠杆菌细胞分裂过程中,Min蛋白系统的振荡参与了小体的正确中细胞放置。基于Min系统的分子相互作用,我们制定了一个数学模型,该模型可在细胞生长和分裂过程中复制Min模式。具体而言,随着膜自身浓度的增加,附着在膜上的MinD停留时间的增加是由膜结合的MinD的二聚作用及其与MinE的相互作用引起的。该系统的仿真在实验和理论MinD分布的波形之间产生了无与伦比的相关性,表明物理系统的主导相互作用已成功地纳入模型中。对于用GFP完全标记MinD的细胞,该模型再现了短细胞的MinD-GFP的固定定位,随后是较大细胞中从极到极的振荡,以及在细胞丝化过程中过渡到对称分布。包含第二个,GFP标记的MinD的细胞显示出对比模式。该模型能够通过增加控制MinD ATPase和异四聚体解离的速率常数来解决这些差异,包括分裂前的临时中细胞定位。对于这两种实验条件,该模型都可以解释细胞分裂如何导致两个子细胞中MinD和MinE的均等分布,并解释了Min振荡周期的温度依赖性。因此,我们表明虽然可能存在其他相互作用,但在体内重现Min系统的主要特征并不需要它们。

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