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裂殖酵母细胞分裂周期的数学模型。

Mathematical model of the cell division cycle of fission yeast.

作者信息

Novak Bela, Pataki Zsuzsa, Ciliberto Andrea, Tyson John J.

机构信息

Department of Agricultural Chemical Technology, Budapest University of Technology and Economics, Szt Gellert ter 4, 1111 Budapest, Hungary.

出版信息

Chaos. 2001 Mar;11(1):277-286. doi: 10.1063/1.1345725.

DOI:10.1063/1.1345725
PMID:12779461
Abstract

Much is known about the genes and proteins controlling the cell cycle of fission yeast. Can these molecular components be spun together into a consistent mechanism that accounts for the observed behavior of growth and division in fission yeast cells? To answer this question, we propose a mechanism for the control system, convert it into a set of 14 differential and algebraic equations, study these equations by numerical simulation and bifurcation theory, and compare our results to the physiology of wild-type and mutant cells. In wild-type cells, progress through the cell cycle (G1-->S-->G2-->M) is related to cyclic progression around a hysteresis loop, driven by cell growth and chromosome alignment on the metaphase plate. However, the control system operates much differently in double-mutant cells, wee1(-) cdc25Delta, which are defective in progress through the latter half of the cell cycle (G2 and M phases). These cells exhibit "quantized" cycles (interdivision times clustering around 90, 160, and 230 min). We show that these quantized cycles are associated with a supercritical Hopf bifurcation in the mechanism, when the wee1 and cdc25 genes are disabled. (c) 2001 American Institute of Physics.

摘要

关于控制裂殖酵母细胞周期的基因和蛋白质,我们已经了解很多。这些分子成分能否组合成一个连贯的机制,来解释裂殖酵母细胞中观察到的生长和分裂行为呢?为了回答这个问题,我们提出了一种控制系统机制,将其转化为一组14个微分方程和代数方程,通过数值模拟和分岔理论研究这些方程,并将我们的结果与野生型和突变型细胞的生理学进行比较。在野生型细胞中,细胞周期进程(G1→S→G2→M)与围绕滞后环的循环进程相关,该进程由细胞生长和中期板上的染色体排列驱动。然而,在双突变细胞wee1(-) cdc25Delta中,控制系统的运作方式却大不相同,这些细胞在细胞周期的后半段(G2和M期)进程中存在缺陷。这些细胞表现出“量化”的周期(分裂间隔时间聚集在90、160和230分钟左右)。我们表明,当wee1和cdc25基因失活时,这些量化周期与该机制中的超临界霍普夫分岔有关。(c)2001美国物理研究所。

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